Lewy Body Disease - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

LEWY BODY DISEASE A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES J ...

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LEWY BODY DISEASE A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES

J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1

Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Lewy Body Disease: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-497-00660-X 1. Lewy Body Disease-Popular works. I. Title.

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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International, Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on Lewy body disease. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.

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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.

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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health

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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON LEWY BODY DISEASE ................................................................................ 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Lewy Body Disease........................................................................ 6 E-Journals: PubMed Central ....................................................................................................... 13 The National Library of Medicine: PubMed ................................................................................ 13 CHAPTER 2. PATENTS ON LEWY BODY DISEASE............................................................................. 37 Overview...................................................................................................................................... 37 Patent Applications on Lewy Body Disease................................................................................. 37 Keeping Current .......................................................................................................................... 39 CHAPTER 3. BOOKS ON LEWY BODY DISEASE ................................................................................ 41 Overview...................................................................................................................................... 41 Book Summaries: Federal Agencies.............................................................................................. 41 Chapters on Lewy Body Disease .................................................................................................. 42 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 47 Overview...................................................................................................................................... 47 NIH Guidelines............................................................................................................................ 47 NIH Databases............................................................................................................................. 49 Other Commercial Databases....................................................................................................... 51 APPENDIX B. PATIENT RESOURCES ................................................................................................. 53 Overview...................................................................................................................................... 53 Patient Guideline Sources............................................................................................................ 53 Finding Associations.................................................................................................................... 55 APPENDIX C. FINDING MEDICAL LIBRARIES .................................................................................. 57 Overview...................................................................................................................................... 57 Preparation................................................................................................................................... 57 Finding a Local Medical Library.................................................................................................. 57 Medical Libraries in the U.S. and Canada ................................................................................... 57 ONLINE GLOSSARIES.................................................................................................................. 63 Online Dictionary Directories ..................................................................................................... 63 LEWY BODY DISEASE DICTIONARY ...................................................................................... 65 INDEX ................................................................................................................................................ 93

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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with Lewy body disease is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about Lewy body disease, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to Lewy body disease, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on Lewy body disease. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to Lewy body disease, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on Lewy body disease. The Editors

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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.

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CHAPTER 1. STUDIES ON LEWY BODY DISEASE Overview In this chapter, we will show you how to locate peer-reviewed references and studies on Lewy body disease.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and Lewy body disease, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “Lewy body disease” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •

Psychiatric Features in Diffuse Lewy Body Disease: A Clinicopathologic Study Using Alzheimer's Disease and Parkinson's Disease Comparison Groups Source: Neurology. 47(5): 1148-1152. November 1996. Summary: This article describes a retrospective study conducted to determine the frequency of depression, hallucinations, and delusions in patients with diffuse Lewy body disease (DLBD) and to compare these findings with those in Alzheimer's disease (AD) and Parkinson's disease (PD). Participants included 112 people. Of these, 28 subjects were diagnosed with DLBD, 58 with AD, and 26 with PD at autopsy. Main outcome measures included the percentages of subjects in each of the three categories in whom depression, hallucinations, or delusions were reported at any time during the course of the illness. Hallucinations and delusions were further classified by type. The

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authors found that depression was more common in DLBD than in AD. There was no difference in the frequency of depression in DLBD and PD. Hallucinations were reported more frequently in DLBD than in AD. There was no difference in the frequency of hallucinations in DLBD and PD. Also, there was no difference in the frequency of delusions in DLBD and AD. There was a male predominance of DLBD cases and PD cases; AD cases were predominantly women. The authors conclude that psychiatric features are very common in DLBD and they should become a central diagnostic criterion for the disease. 1 table, 27 references. (AA-M). •

Accuracy of the Clinical Diagnoses of Lewy Body Disease, Parkinson Disease, and Dementia With Lewy Bodies: A Clinicopathological Study Source: Archives of Neurology. 55: 969-978. July 1998. Summary: This article describes a study to determine early diagnostic predictors as well as the accuracy of the diagnoses of Lewy body disease (LBD), Parkinson's disease (PD), and dementia with Lewy bodies (DLB) by validating the clinical diagnoses of six neurologists with the neuropathologic findings. Data showed that inter-rater reliability for the diagnoses of LBD and PD was moderate for the first visit and substantial for the last; agreement for diagnosis of DLB was fair for the first visit and slight for the last. The raters' results were similar to those of the primary neurologists. Researchers found several features that differentiated PD from DLB, predicted each disorder, and could be used as clinical pointers. Researchers concluded that the low positive predictive value (PPV) with relatively high sensitivity for the diagnosis of PD suggests overdiagnosis; and the extemely low sensitivity for the diagnosis of DLB suggests underdiagnosis. This study confirms features suggested to predict the studied disorders-with the exception of the early presence of postural imbalance, which is not indicative of LBD, PD, or DLB. 2 tables, 91 references (AA-M).

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REM Sleep Behavior Disorder and Degenerative Dementia: An Association Likely Reflecting Lewy Body Disease Source: Neurology. 51: 363-370. August 1998. Summary: This article describes a study to prove the hypothesis that dementia with Lewy Bodies is the underlying disorder in patients with rapid eye movement (REM) sleep behavior disorder (RBD) and degenerative dementia. Researchers studied 37 patients with degenerative dementia and a history of RBD. Patients with and without two or more signs of parkinsonism were compared; parkinsonism occurred in 54 percent of this sample. No statistically significant differences in the frequency of clinical features or in neuropsychological performance appeared between patients with and without parkinsonism. Researchers found that 92 percent of the patients met criteria for clinically possible or probable DLB. Brains of three autopsied patients showed Lewy bodies. Although additional clinicopathologic studies are necessary to confirm the hypothesis that the underlying pathology in these patients is DLB, these findings add weight to it. The authors state that further study is warranted to determine whether the combination of RBD and dementia is more sensitive and specific than the current Consortium on Dementia with Lewy Body criteria. 1 figure, 3 tables, 45 references.

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Probable Diffuse Lewy Body Disease Presenting as REM Sleep Behavior Disorder Source: Neurology. 49: 523-527. August 1997. Summary: This journal article describes a case report of probable diffuse Lewy body disease (DLBD) appearing as rapid eye movement (REM) sleep behavior disorder. A

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right-handed man, age 72 years, presented with a 17-year history of progressive abnormal behavior and violence during sleep. An overnight video polysomnogram revealed increased tonic electromyographic activity during REM sleep and behavior consistent with REM sleep behavior disorder. A progressive cognitive dysfunction began about 15 years after the patient experienced his first sleep disturbance. Over the next 2 years, the patient exhibited progressive dementia, mild parkinsonism, visual hallucinations, illusions, delusions, and striking fluctuations of cognition that were not explained by medical illness. These features met the operational criteria for a clinical diagnosis of DLBD. The authors suggest that the differential diagnosis of progressive neurodegenerative disorders presenting as REM sleep behavior disorder should now include DLBD. 2 figures, 1 table, 30 references. •

Lewy Body Diseases With Dementia: Pathophysiology and Treatment Source: Brain and Cognition. 28: 266-280. 1995. Summary: This journal article discusses the neurobiological processes involved in the dementias associated with Lewy body disease, and potential treatments targeting those processes. The first part reviews the morphological and biochemical characteristics of Lewy bodies, and describes the pathogenetic processes underlying four Lewy body diseases associated with dementia: Parkinson's disease (PD), PD with Alzheimer's disease (AD), cortical Lewy bodies and neuritic plaques, and cortical Lewy body disease (without concomitant AD). The second part examines potential treatments targeting these pathogenetic mechanisms. Two general classes of agents are discussed. One class includes agents which improve current cognitive function by compensating for a chemical deficiency or improving cellular function, such as neurotransmitter replacement therapies and possibly nootropics. The second class includes agents which intervene in the pathogenetic cascade that leads to cell death, such as neuroprotective drugs, antiamyloid agents, and drugs that might interfere with the formation of ADtype pathology. 2 tables, 69 references.

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Antemortem Diagnosis of Diffuse Lewy Body Disease Source: Neurology. 40(10): 1523-1528. October 1990. Summary: Using the presence of widespread cortical Lewy bodies (LB) as the pathologic criteria of diffuse Lewy body disease (DLBD), the authors describe serial neurologic and mental status examinations in 6 patients with DLBD, 3 patients with Alzheimer's disease, and 1 patient with Parkinson's disease. The 6 patients with DLBD included 3 with neocortical neurofibrillary tangles consistent with coincident Alzheimer's disease. Most patients with DLBD had gait impairment concurrent with mild to moderate dementia. Abnormalities of tone or resting tremor were also prominent early symptoms in the subjects with DLBD, but not Alzheimer's disease. patient with DLBD frequently had abnormal EEGs with background posterior slowing and a frontally dominant burst pattern at the time of mild to moderate dementia. Agitation, hallucinations, and delusions were frequent early symptoms in DLBD patients. Patients with DLBD without concomitant Alzheimer's disease had numerous Alz-50 negative cortical plaques. Patients with DLBD have a distinct clinical syndrome that can be differentiated from Alzheimer's disease. Pathologic features, including the absence of Alz-50 immunoreactivity, also differentiate DLBD from Alzheimer's disease. 41 references. (AA).

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Federally Funded Research on Lewy Body Disease The U.S. Government supports a variety of research studies relating to Lewy body disease. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to Lewy body disease. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore Lewy body disease. The following is typical of the type of information found when searching the CRISP database for Lewy body disease: •

Project Title: ALZHEIMERS DISEASE RESEARCH CENTER Principal Investigator & Institution: Thal, Leon J.; Professor and Chair; Neurosciences; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2002; Project Start 28-SEP-1984; Project End 31-MAR-2004 Summary: This proposal is for a five-year renewal of the Alzheimer's Disease Research Center (ADRC) at the University of California San Diego in consortium with The Salk and The Burnham Institutes. The major goals of the Center over the next five years will be to expand our efforts into early clinical identification of Alzheimer's disease (AD) and studying mechanisms of neurodegeneration and repair. Projects will focus on semantic memory in AD, potential mechanisms of neurodegeneration in AD, alpha-synuclein biology, and mechanisms whereby hormones or environment may enhance neuronal survival. In addition, we will continue to carry out detailed clinicopathological correlations and studies of the course of AD. This Center will continue to maintain extremely strong Clinical and Neuropathology Cores. The Clinical Core will continue to longitudinally characterize a cohort of approximately 475-500 subjects to study early changes in cognition and semantic memory, and to provide other AD investigators and the San Diego community as a whole with a well- characterize clinical cohort of both Caucasian and Hispanic volunteer who undergo annual evaluations and are willing to participate in clinical research. The Clinical Core will also recruit special subjects and controls to support the special needs of many of the individual projects. Subjects will also participate in multi-center drug trials. Data derived from subjects will be used in collaborative research. We will place increasing emphasis in identifying genetic influence that either accelerate or protect individuals from the development of AD. In addition, we will continue to focus our studies on the 15-20% of individuals with AD who also have Lewy bodies in their cortex and represent the second most common form of dementia in the United States. The Neuropathology ore will continue to refine the diagnosis of AD and LBD, provide diagnoses, clinicopathological correlations, and brain tissue. The Center as a whole will continue to provide brain tissue, fibroblasts, plasma, DNA, and cerebrospinal fluid to investigators upon request. The ADRC provides a

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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).

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setting to facilitate research training of investigators and will transfer information to the profession and lay communities through our mini-residency program, conferences and other educational activities. The Biostatistics Core will continue to modernize the database and will: 1) maintain the database for the Center, 2) transmit data as requested for the Alzheimer's Disease Data Coordinating Center, 3) provide consultations and statistical expertise for projects emanating from the cores, projects and pilots. Our specific research projects in this renewal include: the role of caspase cleavage in neurodegenerative disease (Bredesen), regulation of neurogenesis in the adult mammalian hippocampus (Gage), NACP/alpha-synuclein and the mechanism of neurodegeneration in Lewy body disease (Masliah), cognitive studies of semantic memory in AD (Salmon), and estrogen mediated neuronal plasticity in the brain (Tuszynski). A mechanism is also outlined for the awarding of pilot feasibility studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CAUSES AGGREGATION

AND

CONSEQUENCES

OF

ALPHA-SYNUCLEIN

Principal Investigator & Institution: Masliah, Eliezer; Professor; J. David Gladstone Institutes Box 419100, 365 Vermont St San Francisco, Ca 94103 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: Parkinson's disease (PD) and related Lewy body diseases are associated with the abnormal intraneuronal accumulation of alpha-synuclein. Mutations that enhance the propensity of alpha-synuclein to aggregate cause early onset familial PD. Notably, the majority of patients with Alzheimer's disease (AD) also have alpha-synuclein immunoreactive Lewy bodies and a substantial proportion of them develop a form of parkinsonism that defies conventional therapeutic approaches. This suggests that factors involved in the pathogenesis of AD might promote the development of particularly recalcitrant forms of PD. We have shown that amyloid beta peptides (Abeta), which play a central role in AD pathogenesis, promote the intracellular accumulation of alphasynuclein and accelerate alpha-synuclein-dependent motor deficits in alphasynuclein/amyloid precursor protein transgenic mice, an animal model that mimics aspects of Lewy body disease. However, the mechanisms underlying these effects remain unknown. The main objectives of this proposal are to elucidate these mechanisms and to determine whether blocking Abeta effects might prevent or ameliorate PD and other Lewy body diseases. In Aim 1 we will determine whether the increase in neuronal alpha-synuclein accumulation and in alpha-synuclein-dependent deficits in a transgenic mouse model of Lewy body disease depends on the ratio of the two predominant Abeta species (Abeta1-42/Abeta1-40). For this purpose, alphasynuclein transgenic mice will be crossed with wildtype or mutant human amyloid precursor protein (hAPP) transgenic mice and detailed biochemical, neuropathological and behavioral analysis will be performed. These experiments will be complemented with in vitro studies in alpha-synuclein-transfected cell fines treated with Abeta1-42 or Abeta1-40 or a mixture of both. In Aim 2 we will determine whether the increase in neuronal alpha-synuclein accumulation and in alpha-synuclein-dependent deficits in a transgenic mouse model of Lewy body disease depends on the uptake of secreted Abeta via the LDL receptor-related protein (LRP). For this purpose, mice expressing both alpha-synuclein and wildtype or mutant hAPP will be crossed with receptor associated protein-deficient mice, which have reduced LRP expression. These experiments will be complemented with in vitro studies in alpha-synuclein-transfected cell lines. In Aim 3 we will determine whether Abeta-dependent alpha-synuclein aggregation and alphasynuclein-dependent neuronal deficits can be reduced by antioxidants. For this purpose,

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alpha-synuclein/hAPP mice will be crossed with superoxide dismutase 1 or 2 transgenic mice. These experiments will be complemented with in vitro studies in synucleintransfected cell lines treated with antioxidants. These experiments will shed light on the overlap between AD and PD and on the role of hAPP/Abeta in the pathogenesis of PD and other Lewy body diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CORE--NEUROPATHOLOGY Principal Investigator & Institution: Hansen, Lawrence A.; Associate Professor; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2002 Summary: The neuropathology core is maintained by a professional staff of Lawrence A. Hanson, M.D. and Eliezer Masliah, M.D. The core will provide post- mortem diagnoses on brain from demented and normal aged control patients clinically evaluated by the San Diego ADRC and maintain a brain tissue bank of formalin fixed and frozen brain tissue from such clinically and neuropathologically characterized patients. Diagnoses will be assigned in accordance with the new neuropathological criteria recently developed the NIA-Regan Institute Working Group. More detailed neuropathologic profiling on each specimen for research purposes will also entail quantification of neocortical and hippocampal plaques and tangles, immunohistochemical stains for amyloid, tau, and ubiquitin, and Braak staging. On the basis of past experience, we anticipate receiving 40 brains annually. In some cases, rapid autopsies (within 8 hours of death) allow fresh brain tissue to be distributed to ADRC affiliated research laboratories for use in RNA biochemistry, in situ section in the midline with the neuropathologic evaluation of the left hemibrain and freezing of the right hemibrain for distribution of frozen brain tissue to other investigators within and outside the ADRC. The standard neuropathological protocol includes H&E, thioflavin-S, anti-amyloid, anti-tau, and antiubiquitin preparations of frontal, temporal and parietal lobes, anterior and posterior hippocampus, substantia innominata, mesencephalon, and pons. Lewy body disease is evaluated with both H&E and anti-ubiquitin immunohistochemical preparations. Cresyl violet stained sections are used for neocortical morphometry and image analysis. ChAT activity and synaptophysin measurements are performed to support specific projects. All data are recorded in the computerized database of this core as well as in the ADRC main computer, and can be shared with other ADDCC centers upon request. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EPIDEMIOLOGY OF BRAIN AGING IN THE VERY OLD Principal Investigator & Institution: White, Lon R.; Professor of Epidemiology; Kuakini Medical Center 347 N Kuakini St Honolulu, Hi 96817 Timing: Fiscal Year 2002; Project Start 01-SEP-2001; Project End 31-AUG-2006 Summary: We have three fundamental aims: (1) to examine relationships of structural brain characteristics determined at autopsy with clinical diagnoses, cognitive function, and motor function in the years and months prior to death, (2) to assess associations of candidate risk factors with incident mild cognitive impairment (MCI), Alzheimer's disease (AD), vascular dementia (VsD), extrapyramidal motor signs (EMS), and Parkinson's disease (PD), and (3) to estimate age-specific incidence rates for these same endpoints, extending existing estimates into the tenth decade of life. These will be accomplished by continuing operation of the Honolulu-Asia Aging Study (HAAS) through two full examination cycles, providing new cases for analysis in combination

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with recently identified incident cases. All accrued data and materials will be added to the existing NIA-Kuakini HAAS Archive, to be made available to collaborating scientists at the NIA and at other extramural sites, to 'facilitate preservation and future utilization of this unique resource. Our structure-function research is focused on 4 major, distinct, aging-related structural brain changes: the Alzheimer process (indicated by neurofibrillary tangles and neuritic plaques), cerebrovascular disease (infarcts and arterial wall architecture), aging-related atrophy (general and regional), and the Lewy body process (associated with nigral degeneration, PD, EMS, and cortical Lewy body disease). Each endpoint is envisioned as linked most strongly to one of these, with variable contributions from one or more of the others. The risk factor research will include: examination of factors previously identified as associated with prevalent endpoints for their associations with incident endpoints; a search for "new" risk factors using information collected between 1986-93; and evaluation of recent data from Polysomnography, tests of olfaction, and tests of reaction time as indicators of incipient or imminent AD or PD. A closely related NIA grant will support autopsy acquisition, conduct, and data management activities related to neuropathology from June 1, 2000 through May 30, 2005. NIA contract support of current HAAS operations is scheduled to end June 30, 2001. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PROTEOMIC STUDIES IN PARKINSON'S DISEASE Principal Investigator & Institution: Zhang, Jing; Pathology; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2004; Project Start 07-JUL-2004; Project End 30-APR-2009 Summary: (provided by applicant): Parkinson's disease is a common age-related neurodegenerative disease characterized pathologically by a loss of dopaminergic neurons in the substantia nigra with resultant depletion of striatal dopamine and presence of Lewy bodies in the remaining neurons. Lewy body contains numerous functional and structural proteins, including alpha-synuclein and ubiquitin, and aggregation of alpha-synuclein is thought to be important in Lewy body formation as well as neurodegeneration, although the detailed mechanisms remain to be defined. Increasing evidence has suggested that mitochondrial dysfunction, increased oxidative stress and dysfunction of the ubiquitin-proteasome system may be involved in Lewy body formation as well as neurodegeneration. A few neurotoxicants, e.g. rotenone, 1methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine, all capable of inhibiting mitochondria and enhancing oxidative stress, have been utilized widely to generate parkinsonian models in vitro and in vivo. Interestingly only rotenone produces Lewy body-like cytoplasmic inclusions. On the other hand, there are also human nigral degenerative diseases with or without Lewy body formation in the substantia nigra, including Parkinson's disease, dementia with Lewy body disease and multiple system atrophy. Our preliminary studies in cell cultures demonstrated that proteins interacting with alpha-synuclein may influence alpha-synuclein aggregation, Lewy body formation and cell death. Hence, this application proposes to advance our understating of the development of Lewy bodies as well as molecular mechanisms of development of Parkinson's disease with subtractive proteomics by looking for differences in the proteins associated with alpha-synuclein in the substantia nigra between rotenoneexposed and control rats first, and then comparing the protein profiles in rotenoneexposed rats vs. rats exposed to 1- methyl-4-phenylpyridinium, the active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, or 6- hydroxydopamine. A second phase would examine tissues from patients with Parkinson's disease vs. controls as well as

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patients with multiple system atrophy. Finally, we will study the roles of the common and differentially displayed proteins, those related to oxidative stress, mitochondrial and proteosomal function in particular, in alpha-synuclein aggregation, Lewy body formation and neurodegeneration. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PROTEOPATHIES OF THE AGING CENTRAL NERVOUS SYSTEM Principal Investigator & Institution: Mucke, Lennart; Associate Professor; J. David Gladstone Institutes Box 419100, 365 Vermont St San Francisco, Ca 94103 Timing: Fiscal Year 2003; Project Start 15-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): We will address the hypothesis that different neurodegenerative diseases are caused by the accumulation of distinct proteins with pathogenic conformations (proteopathies). These disorders are a complex biomedical, behavioral, and social problem as they are increasing in frequency, cause major disability, and remain largely untreatable. If the ways in which different proteins damage nerve cells overlap, treatments may be developed to prevent and reverse more than one of these conditions. We have assembled five interactive projects and four essential cores to study the mechanisms by which proteins associated with Alzheimer's, Parkinson's, or Huntington's disease impair neuronal function and survival. The program is multidisciplinary and relies on state-of the-art technology, including X-ray crystallography, robotic microscopy, transgenic and gene-targeted mouse models, cellular biology, neuropathology, and behavioral neuroscience. Project 1, "Polyglutamine Conformation and Neurodegeneration," aims to differentiate whether visible aggregates or other conformational states of mutant huntingtin are responsible for Huntington's disease-related neurodegeneration. Project 2, "Protein Structure in Apolipoprotein E4-associated Neurodegeneration," will test whether the Alzheimer's disease-promoting effect of apolipoprotein E4 depends on the conformation and stability of this molecule. Project 3, "Apolipoprotein E in Neurobiology: Cellular Mechanisms," will examine whether apolipoprotein E4 promotes Alzheimer's diseaselike pathology through amyloid beta peptide (Abeta)-dependent pathways or via independent mechanisms. Project 4, "Causes and Consequences of alpha-Synuclein Aggregation," will assess whether pathogenic interactions between Abeta and alphasynuclein could contribute to the development of Parkinson's disease and other Lewy body diseases. Project 5, "Mechanisms of AbetaD-induced Neuronal Deficits," will analyze the molecular cascades that link the formation of neurotoxic Abeta assemblies to Alzheimer's disease-related cognitive decline and test whether these cascades can be modulated by apolipoprotein E isoforms and alpha-synuclein. The Cores (A: Administrative; B: Tissue Culture; C: Animal; D: Neuropathology/Imaging) will provide the common services necessary to accomplish the goals of the program project. Our studies will shed light on diverse neurodegenerative diseases and could provide the knowledge needed to better treat and prevent them. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ROLE OF ALPHA SYNUCLEIN IN LEWY BODY DISEASE Principal Investigator & Institution: Hyman, Bradley T.; Professor; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SLEEP, CIRCADIAN RHYTHMS AND DEMENTING ILLNESSES Principal Investigator & Institution: Harper, David G.; Mc Lean Hospital (Belmont, Ma) Belmont, Ma 02478 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): Sleep disturbance is a disruptive symptom shared by the spectrum of progressive dementing illnesses, and its presence often precipitates decisions by families to seek institutional care for patients. Normal sleep-wake regulation is characterized by an oscillatory, circadian, alerting process and a linear, sleep-inducing process building need to sleep as a function of the duration of prior wakefulness. In our previous studies in this population, we have found diagnosisspecific circadian abnormalities in men, which implicate central, circadian dysfunction in the etiology of sleep-wake disturbance in Alzheimer's disease, frontotemporal degeneration, and Lewy body disease. In addition, we have found abnormalities in SCN cellular populations in men linked with specific circadian and behavioral changes in Alzheimer's disease. We now wish to build upon these initial findings and expand our studies to the extra-SCN circadian system as well as the SCN itself. We propose for this funding period to test four hypotheses. 1) Polysomnographic sleep in AD will be more disturbed in patients with large phase-delays of their circadian core-body temperature rhythm characterized by reduced sleep efficiency add longer sleep latency. Sleep will be more fragmented in patients with FTD compared to AD patients with an increased number of awakenings. 2) Female patients with probable AD will have similady delayed phase of temperature and activity as male patients and normal controls; 3) Noctumal agitation and restlessness, seen in AD, results from loss of serotonergic innervation of the suprachiasmatic nuclei and will be detectable as lower RIA serotonin transporter protein (5-HTT) in SCN compared to FTD patients and controls. In addition, measurements of nocturnal agitation will be higher in AD patients with lower 5-HTT; and 4) Patients with FTD wilt have lowered levels of orexin/hypocretin in target tissue of perifonical area of the hypothalamus, locus coeruleus, midline thalamus and/or dorsal raphe nuclei compared to AD and controls. The extent of dissociation of activity and temperature will be related to the 10ss of orexin/hypocretin in patients carrying the same dementia diagnoses. To accomplish these objectives we will study patients with progressive dementing illnesses collecting core-body temperature, polysomnographic and locomotor activity data every 6 months and followed by post-mortem neuropathological studies in addition to diagnosis-based neuropathological studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: UBIQUITINATION/RECEPTOR SIGNALING--REGULATION BY PARKIN Principal Investigator & Institution: Wolozin, Benjamin L.; Professor; Pharmacol & Exper Therapeutics; Loyola University Chicago Lewis Towers, 13Th Fl Chicago, Il 60611 Timing: Fiscal Year 2002; Project Start 01-JUN-2001; Project End 31-MAY-2005 Summary: (Provided by Applicant): Mutations in the gene coding for Parkin cause a rare familial form of Parkinsonism, autosomal recessive juvenile Parkinsonism, that results in death of dopaminergic neurons in the substantia nigra. To understand how parkin causes disease, we need to understand the regulation and function of parkin. Our studies have lead us to investigate ubiquitination, which is a process that regulates protein degradation. We hypothesize that parkin regulates ubiquitination of other proteins in response to cellular contact with matrix proteins (such as collagen and

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laminin), and thereby controls regulation of the cytoskeleton and signal transduction by matrix proteins and their integrin receptors. Loss of parkin function could cause neurodegeneration by inhibiting matrix signaling and impairing maintenance of processes by neurons. Our preliminary data support this hypothesis by demonstrating that parkin-dependent ubiquitination is activated by cellular binding to matrix proteins. We have also identified parkin binding proteins that are associated with integrins. Conversely, cell lines that have reduced parkin expression (due to anti-sense parkin cDNA) decrease ubiquitination, retract processes upon cellular exposure to matrix proteins, and have abnormal signal transduction. The goal of this proposal is to investigate the regulation of ubiquitination by parkin (Aim 1), determine the role of parkin in regulating signaling in response to exposure of cells to matrix proteins (Aim 2) and identify common functional deficits associated with disease-related mutations in parkin. Interestingly, parkin is also linked to other forms of neurodegeneration. Parkin binds to alpha-synuclein, and in brains from donors with Parkinson's disease parkin accumulates in inclusions that contain alpha-synuclein, and shows 75% less binding of parkin to two proteins, filamin and hCDCrel2a. We intend to investigate the mechanism of parkin dysfunction by determining how parkin function is altered in Lewy body diseases, and whether oxidation or alpha-synuclein aggregation causes the dysfunction of parkin (Aim 3). The research in this proposal will provide insight into the function of parkin, determine how mutations in parkin produce disease, and provide a new window to understand the molecular pathophysiology of Parkinson's disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VARIAN 4 TESLA MRI/MRS FOR NEURO-DEGENERATIVE DISEASES Principal Investigator & Institution: Weiner, Michael W.; Professor of Medicine, Radiology, Psychi; Northern California Institute Res & Educ 4150 Clement Street (151Nc) San Francisco, Ca 941211545 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-MAR-2004 Summary: (provided by applicant): This application requests a Varian 4 Tesla MRI/MRS(I) system to continue our 15-yr focus on investigation of neurodegenerative diseases (ND). Goals, to: 1) determine the pathophysiology of various ND including cross sectional and longitudinal changes of anatomic (i.e. spatial) patterns of brain structure, perfusion, and metabolites; 2) develop improved diagnostic methods which can be applied to clinical practice; 3) develop methods for staging and monitoring disease progression which can be used in treatment trials; and 4) detect ND at an early, preclinical stage so that preventative treatment can be effectively initiated. This is a continuation of collaborative work between MR physicists, who develop new MRI/MRS(I) techniques, and clinical investigators. We believe that we have done more MRI/MRS(I) of ND than any other group in the world (> 2500 subjects/ 8 yrs). Our physicists have developed many new MRS(I) techniques (pulse sequences, RF pulses, coils, data processing); this emphasizes their ability to develop 4T techniques aimed at ND. Our clinical collaborators have funded projects on normal aging, Alzheimer's disease, frontotemporal dementia, vascular dementia, Lewy Body disease, epilepsy, Parkinson's disease, amyotrophic lateral sclerosis, post traumatic stress disorder, schizophrenia, bipolar disorder, HN, alcoholism, and gulf war illness. Each project uses quantified MRI/MRS(I) data together with clinical/cognitive measures to test hypotheses statistically. Benefits of an increased field from 1.5-4T: Improved sensitivity for MRI in detecting anatomical change because of increased contrast as well as improved perfusion and diffusion MRI due to longer T1; Improved MRS(I) because of 3-

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fold increased S/N, allowing increased accuracy, smaller voxels, and increased spectral dispersion, facilitating measurement of glutamate (implicated in neurodegeneration), GABA, and other metabolites. ND has growing importance because of the aging population. Improved understanding of ND has led to development of new treatments and clinical trials. This project will focus advanced MRI/MRS(I) techniques at 4T on ND in order to increase knowledge concerning pathophysiology of ND, improve diagnosis and treatment monitoring, and finally to detect ND before debilitating symptoms develop, allowing preventative measures. These expected results emphasize the practical outcome and significance of this research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “Lewy body disease” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for Lewy body disease in the PubMed Central database: •

Assessment of diffuse Lewy body disease by 2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography (FDG PET). by Mirzaei S, Knoll P, Koehn H, Bruecke T.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151666

The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with Lewy body disease, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “Lewy body disease” 3 4

Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.

With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print. 6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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(or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for Lewy body disease (hyperlinks lead to article summaries): •

14-3-3 proteins in Lewy bodies in Parkinson disease and diffuse Lewy body disease brains. Author(s): Kawamoto Y, Akiguchi I, Nakamura S, Honjyo Y, Shibasaki H, Budka H. Source: Journal of Neuropathology and Experimental Neurology. 2002 March; 61(3): 245-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11895039

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A 99mTc-HMPAO single-photon emission computed tomography study of Lewy body disease. Author(s): Varma AR, Talbot PR, Snowden JS, Lloyd JJ, Testa HJ, Neary D. Source: Journal of Neurology. 1997 June; 244(6): 349-59. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9249619

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A case of Down's syndrome with diffuse Lewy body disease and Alzheimer's disease. Author(s): Bodhireddy S, Dickson DW, Mattiace L, Weidenheim KM. Source: Neurology. 1994 January; 44(1): 159-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8290054

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A common NURR1 polymorphism associated with Parkinson disease and diffuse Lewy body disease. Author(s): Zheng K, Heydari B, Simon DK. Source: Archives of Neurology. 2003 May; 60(5): 722-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12756136

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A generalised increase in protein carbonyls in the brain in Parkinson's but not incidental Lewy body disease. Author(s): Alam ZI, Daniel SE, Lees AJ, Marsden DC, Jenner P, Halliwell B. Source: Journal of Neurochemistry. 1997 September; 69(3): 1326-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9282961

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A neuropathological subset of Alzheimer's disease with concomitant Lewy body disease and spongiform change. Author(s): Hansen LA, Masliah E, Terry RD, Mirra SS. Source: Acta Neuropathologica. 1989; 78(2): 194-201. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2546359

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A pathological study of the association between Lewy body disease and Alzheimer's disease. Author(s): Gibb WR, Mann DM, Mountjoy CQ, Lees AJ. Source: Adv Neurol. 1990; 53: 55-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2173375

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A pathological study of the association between Lewy body disease and Alzheimer's disease. Author(s): Gibb WR, Mountjoy CQ, Mann DM, Lees AJ. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1989 June; 52(6): 701-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2545826

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A review of Lewy body disease, an emerging concept of cortical dementia. Author(s): Papka M, Rubio A, Schiffer RB. Source: The Journal of Neuropsychiatry and Clinical Neurosciences. 1998 Summer; 10(3): 267-79. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9706534

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Abnormal alpha-synuclein interactions with rab3a and rabphilin in diffuse Lewy body disease. Author(s): Dalfo E, Barrachina M, Rosa JL, Ambrosio S, Ferrer I. Source: Neurobiology of Disease. 2004 June; 16(1): 92-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15207266

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Abnormal distribution of the non-Abeta component of Alzheimer's disease amyloid precursor/alpha-synuclein in Lewy body disease as revealed by proteinase K and formic acid pretreatment. Author(s): Takeda A, Hashimoto M, Mallory M, Sundsumo M, Hansen L, Sisk A, Masliah E. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 1998 September; 78(9): 1169-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9759660

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Abnormal, ubiquitinated cortical neurites in patients with diffuse Lewy body disease. Author(s): Pellise A, Roig C, Barraquer-Bordas LI, Ferrer I. Source: Neuroscience Letters. 1996 March 15; 206(2-3): 85-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8710193

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Accumulation of alpha-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy. Author(s): Wakabayashi K, Hayashi S, Kakita A, Yamada M, Toyoshima Y, Yoshimoto M, Takahashi H. Source: Acta Neuropathologica. 1998 November; 96(5): 445-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9829807

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Accumulation of NACP/alpha-synuclein in lewy body disease and multiple system atrophy. Author(s): Shoji M, Harigaya Y, Sasaki A, Ueda K, Ishiguro K, Matsubara E, Watanabe M, Ikeda M, Kanai M, Tomidokoro Y, Shizuka M, Amari M, Kosaka K, Nakazato Y, Okamoto K, Hirai S. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2000 May; 68(5): 605-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10766891

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Accuracy of the clinical diagnoses of Lewy body disease, Parkinson disease, and dementia with Lewy bodies: a clinicopathologic study. Author(s): Litvan I, MacIntyre A, Goetz CG, Wenning GK, Jellinger K, Verny M, Bartko JJ, Jankovic J, McKee A, Brandel JP, Chaudhuri KR, Lai EC, D'Olhaberriague L, Pearce RK, Agid Y. Source: Archives of Neurology. 1998 July; 55(7): 969-78. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9678315

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Aggregation of alpha-synuclein/NACP in the neuronal and glial cells in diffuse Lewy body disease: a survey of six patients. Author(s): Piao YS, Wakabayashi K, Hayashi S, Yoshimoto M, Takahashi H. Source: Clin Neuropathol. 2000 July-August; 19(4): 163-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10919347

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Alpha-synuclein accumulates in Purkinje cells in Lewy body disease but not in multiple system atrophy. Author(s): Mori F, Piao YS, Hayashi S, Fujiwara H, Hasegawa M, Yoshimoto M, Iwatsubo T, Takahashi H, Wakabayashi K. Source: Journal of Neuropathology and Experimental Neurology. 2003 August; 62(8): 812-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14503637

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Alpha-synuclein in Lewy body disease and Alzheimer's disease. Author(s): Hashimoto M, Masliah E. Source: Brain Pathology (Zurich, Switzerland). 1999 October; 9(4): 707-20. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10517509

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Alterations in peptide levels in Parkinson's disease and incidental Lewy body disease. Author(s): Fernandez A, de Ceballos ML, Rose S, Jenner P, Marsden CD. Source: Brain; a Journal of Neurology. 1996 June; 119 ( Pt 3): 823-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8673494

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Alterations of muscarinic acetylcholine receptor subtypes in diffuse Lewy body disease: relation to Alzheimer's disease. Author(s): Jellinger KA. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2000 February; 68(2): 2534. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10702044

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Alterations of muscarinic acetylcholine receptor subtypes in diffuse lewy body disease: relation to Alzheimer's disease. Author(s): Shiozaki K, Iseki E, Uchiyama H, Watanabe Y, Haga T, Kameyama K, Ikeda T, Yamamoto T, Kosaka K. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1999 August; 67(2): 209-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10406992

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Alzheimer's disease and Lewy body disease: a comparative clinicopathological study. Author(s): Lippa CF, Smith TW, Swearer JM. Source: Annals of Neurology. 1994 January; 35(1): 81-8. Erratum In: Ann Neurol 1994 March; 35(3): 380. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8285597

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Alzheimer's disease, Lewy body disease and aging: a comparative study of the perforant pathway. Author(s): Lippa CF, Pulaski-Salo D, Dickson DW, Smith TW. Source: Journal of the Neurological Sciences. 1997 April 15; 147(2): 161-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9106122

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Amyloid angiopathy in diffuse Lewy body disease. Author(s): Wu E, Lipton RB, Dickson DW. Source: Neurology. 1992 November; 42(11): 2131-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1436523

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Amyloid beta-peptide and its relationship with dementia in Lewy body disease. Author(s): Jendroska K, Kashiwagi M, Sassoon J, Daniel SE. Source: Journal of Neural Transmission. Supplementum. 1997; 51: 137-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9470134

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Antemortem diagnosis of diffuse Lewy body disease. Author(s): Crystal HA, Dickson DW, Lizardi JE, Davies P, Wolfson LI. Source: Neurology. 1990 October; 40(10): 1523-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2170865

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Anti-ubiquitin immunocytochemistry is more sensitive than conventional techniques in the detection of diffuse Lewy body disease. Author(s): Lennox G, Lowe J, Morrell K, Landon M, Mayer RJ. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1989 January; 52(1): 67-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2540286

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Apolipoprotein E gene in diffuse Lewy body disease with or without co-existing Alzheimer's disease. Author(s): Arai H, Higuchi S, Muramatsu T, Iwatsubo T, Sasaki H, Trojanowski JQ. Source: Lancet. 1994 November 5; 344(8932): 1307. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7818703

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Apolipoprotein E genotype and Lewy body disease. Author(s): Lippa CF, Smith TW, Saunders AM, Crook R, Pulaski-Salo D, Davies P, Hardy J, Roses AD, Dickson D. Source: Neurology. 1995 January; 45(1): 97-103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7824144

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Apolipoprotein E4 and Alzheimer's disease pathology in Lewy body disease and in other beta-amyloid-forming diseases. Author(s): Pickering-Brown SM, Mann DM, Bourke JP, Roberts DA, Balderson D, Burns A, Byrne J, Owen F. Source: Lancet. 1994 May 7; 343(8906): 1155. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7818636

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Argyrophilic glial inclusions in the midbrain of patients with Parkinson's disease and diffuse Lewy body disease are immunopositive for NACP/alpha-synuclein. Author(s): Arai T, Ueda K, Ikeda K, Akiyama H, Haga C, Kondo H, Kuroki N, Niizato K, Iritani S, Tsuchiya K. Source: Neuroscience Letters. 1999 January 8; 259(2): 83-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10025563

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Atypical diffuse Lewy body disease with neuritic abnormalities. Author(s): Reyes E, Gamboa A, Masliah E. Source: Clin Neuropathol. 1993 November-December; 12(6): 330-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8287626

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Atypical dopa responsive parkinsonism in a patient with megalencephaly, midbrain Lewy body disease, and some pathological features of Hallervorden-Spatz disease. Author(s): Tuite PJ, Provias JP, Lang AE. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1996 November; 61(5): 523-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8937352

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Autosomal dominant diffuse Lewy body disease. Author(s): Wakabayashi K, Hayashi S, Ishikawa A, Hayashi T, Okuizumi K, Tanaka H, Tsuji S, Takahashi H. Source: Acta Neuropathologica. 1998 August; 96(2): 207-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9705138

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Bcl-2 and Bax proteins in Lewy bodies from patients with Parkinson's disease and Diffuse Lewy body disease. Author(s): Tortosa A, Lopez E, Ferrer I. Source: Neuroscience Letters. 1997 November 28; 238(1-2): 78-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9464659

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Brain perfusion scintigraphy with 99mTc-HMPAO or 99mTc-ECD and 123I-beta-CIT single-photon emission tomography in dementia of the Alzheimer-type and diffuse Lewy body disease. Author(s): Donnemiller E, Heilmann J, Wenning GK, Berger W, Decristoforo C, Moncayo R, Poewe W, Ransmayr G. Source: European Journal of Nuclear Medicine. 1997 March; 24(3): 320-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9143472

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Brainstem-type Lewy body disease presenting with progressive autonomic failure and lethargy. Author(s): Hishikawa N, Hashizume Y, Hirayama M, Imamura K, Washimi Y, Koike Y, Mabuchi C, Yoshida M, Sobue G. Source: Clinical Autonomic Research : Official Journal of the Clinical Autonomic Research Society. 2000 June; 10(3): 139-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10954072

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Changes of monoamines in post-mortem brains from patients with diffuse Lewy body disease. Author(s): Ohara K, Kondo N, Ohara K. Source: Progress in Neuro-Psychopharmacology & Biological Psychiatry. 1998 February; 22(2): 311-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9608603

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Clinical and neuropathological aspects of diffuse Lewy body disease in the elderly. Author(s): Kuzuhara S, Yoshimura M. Source: Adv Neurol. 1993; 60: 464-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8420171

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Clinical and neuropathological correlates of Lewy body disease. Author(s): Jellinger KA, Seppi K, Wenning GK. Source: Acta Neuropathologica. 2003 August; 106(2): 188-9; Author Reply 190. Epub 2003 June 03. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12783247

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Clinical and neuropathological correlates of Lewy body disease. Author(s): Hishikawa N, Hashizume Y, Yoshida M, Sobue G. Source: Acta Neuropathologica. 2003 April; 105(4): 341-50. Epub 2003 January 14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12624787

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Clinical and pathological features of diffuse cortical Lewy body disease (Lewy body dementia). Author(s): Gibb WR, Esiri MM, Lees AJ. Source: Brain; a Journal of Neurology. 1987 October; 110 ( Pt 5): 1131-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2823957

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Clinical features of familial diffuse Lewy body disease. Author(s): Ishikawa A, Takahashi H, Tanaka H, Hayashi T, Tsuji S. Source: European Neurology. 1997; 38 Suppl 1: 34-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9276199

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Clinicopathological studies on diffuse Lewy body disease. Author(s): Kosaka K, Iseki E. Source: Neuropathology : Official Journal of the Japanese Society of Neuropathology. 2000 March; 20(1): 1-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10935431

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Close relationship between spongiform change and ubiquitin-positive granular structures in diffuse Lewy body disease. Author(s): Iseki E, Li F, Kosaka K. Source: Journal of the Neurological Sciences. 1997 February 27; 146(1): 53-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9077496

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Clozapine use in diffuse Lewy body disease. Author(s): Chacko RC, Hurley RA, Jankovic J. Source: The Journal of Neuropsychiatry and Clinical Neurosciences. 1993 Spring; 5(2): 206-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8508040

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Coexistent Lewy body disease in a case of "visual variant of Alzheimer's disease". Author(s): Tang-Wai DF, Josephs KA, Boeve BF, Petersen RC, Parisi JE, Dickson DW. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2003 March; 74(3): 389. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12588940

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Comparison of extrapyramidal features in 31 pathologically confirmed cases of diffuse Lewy body disease and 34 pathologically confirmed cases of Parkinson's disease. Author(s): Louis ED, Klatka LA, Liu Y, Fahn S. Source: Neurology. 1997 February; 48(2): 376-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9040725

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Concurrence of Alzheimer's disease, Parkinson's disease, diffuse Lewy body disease, and amyotrophic lateral sclerosis. Author(s): Hedera P, Lerner AJ, Castellani R, Friedland RP. Source: Journal of the Neurological Sciences. 1995 February; 128(2): 219-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7738598

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Cortical changes in the parkinsonian brain: a contribution to the delineation of "diffuse Lewy body disease". Author(s): Yoshimura M. Source: Journal of Neurology. 1983; 229(1): 17-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6189974

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Cortical Lewy body disease. Author(s): Burn DJ. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2004 February; 75(2): 1758. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14742580

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Cyclin-dependent kinase 5 (Cdk5) associated with Lewy bodies in diffuse Lewy body disease. Author(s): Takahashi M, Iseki E, Kosaka K. Source: Brain Research. 2000 April 17; 862(1-2): 253-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10799694

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Cytoskeletal pathology in non-Alzheimer degenerative dementia: new lesions in diffuse Lewy body disease, Pick's disease, and corticobasal degeneration. Author(s): Dickson DW, Feany MB, Yen SH, Mattiace LA, Davies P. Source: Journal of Neural Transmission. Supplementum. 1996; 47: 31-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8841955

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Lewy Body Disease

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Damage to nuclear DNA in Lewy body disease. Author(s): Love S. Source: Neuroreport. 2001 August 28; 12(12): 2725-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11522956

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Defining diffuse Lewy body disease. Tetrad of symptoms distinguishes illness from other dementias. Author(s): Stewart JT. Source: Postgraduate Medicine. 2003 May; 113(5): 71-5; Quiz 3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12764897

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Degenerative terminals of the perforant pathway are human alpha-synucleinimmunoreactive in the hippocampus of patients with diffuse Lewy body disease. Author(s): Iseki E, Marui W, Kosaka K, Akiyama H, Ueda K, Iwatsubo T. Source: Neuroscience Letters. 1998 December 18; 258(2): 81-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9875532

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Dementia and neuropathology in Lewy body disease. Author(s): Kosaka K. Source: Adv Neurol. 1993; 60: 456-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8420170

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Dementia in Parkinson's disease in association with diffuse Lewy body disease. Author(s): Philpot M, Levy R. Source: Lancet. 1987 March 14; 1(8533): 624-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2881155

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Did Don Quixote have Lewy body disease? Author(s): Garcia Ruiz PJ, Gulliksen L. Source: Journal of the Royal Society of Medicine. 1999 April; 92(4): 200-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10450203

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Diffuse Lewy body disease - a clinical syndrome or a disease entity? Author(s): Benecke R. Source: Journal of Neurology. 2003 February; 250 Suppl 1: I39-42. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12761635

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Diffuse Lewy body disease and progressive dementia in a young woman. Author(s): Crowe SF, Peppard RF, Borenstein R, Lloyd JH. Source: The Australian and New Zealand Journal of Psychiatry. 1992 September; 26(3): 507-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1417640

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Diffuse Lewy body disease and progressive dementia. Author(s): Burkhardt CR, Filley CM, Kleinschmidt-DeMasters BK, de la Monte S, Norenberg MD, Schneck SA. Source: Neurology. 1988 October; 38(10): 1520-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2843793

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Diffuse Lewy body disease as substrate of primary lateral sclerosis. Author(s): Hainfellner JA, Pilz P, Lassmann H, Ladurner G, Budka H. Source: Journal of Neurology. 1995 January; 242(2): 59-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7707090

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Diffuse Lewy body disease in Japan. Author(s): Kosaka K. Source: Journal of Neurology. 1990 June; 237(3): 197-204. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2196340

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Diffuse Lewy body disease presenting as multiple system atrophy. Author(s): Pakiam AS, Bergeron C, Lang AE. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 1999 May; 26(2): 127-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10352873

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Diffuse Lewy body disease presenting with a supranuclear gaze palsy. Author(s): Fearnley JM, Revesz T, Brooks DJ, Frackowiak RS, Lees AJ. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1991 February; 54(2): 15961. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1850451

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Diffuse Lewy body disease presenting with supranuclear gaze palsy, parkinsonism, and dementia: a case report. Author(s): de Bruin VM, Lees AJ, Daniel SE. Source: Movement Disorders : Official Journal of the Movement Disorder Society. 1992 October; 7(4): 355-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1484531

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Diffuse Lewy body disease with dementia and oculomotor dysfunction. Author(s): Lewis AJ, Gawel MJ. Source: Movement Disorders : Official Journal of the Movement Disorder Society. 1990; 5(2): 143-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2157979

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Lewy Body Disease

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Diffuse Lewy body disease with immediate post-partum onset. Author(s): Opeskin K, Gonzales M, Borenstein R, Anderson R. Source: Acta Neuropathologica. 1993; 85(2): 213-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8442413

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Diffuse Lewy body disease without amyloid plaques in a patient homozygous for apolipoprotein E allele epsilon 4: a case report. Author(s): Seltzer B, Fratkin J, Clejan S. Source: Journal of Geriatric Psychiatry and Neurology. 1996 October; 9(4): 181-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8970011

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Diffuse Lewy body disease. Author(s): Kosaka K. Source: Neuropathology : Official Journal of the Japanese Society of Neuropathology. 2000 September; 20 Suppl: S73-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11037193

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Diffuse Lewy body disease. Author(s): Kosaka K. Source: Intern Med. 1998 January; 37(1): 6-10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9510392

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Diffuse Lewy body disease. Author(s): Lennox G, Lowe J, Byrne EJ, Landon M, Mayer RJ, Godwin-Austen RB. Source: Lancet. 1989 February 11; 1(8633): 323-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2563473

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Diffuse Lewy body disease. Neuropathological and biochemical studies of six patients. Author(s): Dickson DW, Davies P, Mayeux R, Crystal H, Horoupian DS, Thompson A, Goldman JE. Source: Acta Neuropathologica. 1987; 75(1): 8-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3434218

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Diffuse Lewy body disease: a common yet misdiagnosed dementia in which neuroleptics may be contraindicated. Author(s): Scarbrough TJ. Source: Tenn Med. 1998 February; 91(2): 58-60. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9478123

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Diffuse Lewy body disease: an autopsy case. Author(s): Kuroda S, Otsuki S, Hayashi Y. Source: Acta Medica Okayama. 1987 June; 41(3): 133-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2820201

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Diffuse Lewy body disease: an important differential diagnosis in dementia with extrapyramidal features. Author(s): Lennox G, Lowe JS, Godwin-Austen RB, Landon M, Mayer RJ. Source: Prog Clin Biol Res. 1989; 317: 121-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2602409

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Diffuse Lewy body disease: clinical features in 15 cases. Author(s): Byrne EJ, Lennox G, Lowe J, Godwin-Austen RB. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1989 June; 52(6): 709-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2545827

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Diffuse Lewy body disease: clinical features in nine cases without coexistent Alzheimer's disease. Author(s): Hely MA, Reid WG, Halliday GM, McRitchie DA, Leicester J, Joffe R, Brooks W, Broe GA, Morris JG. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1996 May; 60(5): 531-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8778258

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Diffuse Lewy body disease: clinical, pathological, and neuropsychological review. Author(s): Luis CA, Mittenberg W, Gass CS, Duara R. Source: Neuropsychology Review. 1999 September; 9(3): 137-50. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10565674

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Diffuse Lewy body disease: correlative neuropathology using anti-ubiquitin immunocytochemistry. Author(s): Lennox G, Lowe J, Landon M, Byrne EJ, Mayer RJ, Godwin-Austen RB. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1989 November; 52(11): 1236-47. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2556498

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Diffuse Lewy body disease: light and electron microscopic immunocytochemistry of senile plaques. Author(s): Dickson DW, Crystal H, Mattiace LA, Kress Y, Schwagerl A, Ksiezak-Reding H, Davies P, Yen SH. Source: Acta Neuropathologica. 1989; 78(6): 572-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2683563

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Diffuse Lewy body disease: the clinical features. Author(s): Byrne EJ, Lennox G, Lowe J, Reynolds G. Source: Adv Neurol. 1990; 53: 283-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2173371

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Diffuse type of Lewy body disease: progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree--a new disease? Author(s): Kosaka K, Yoshimura M, Ikeda K, Budka H. Source: Clin Neuropathol. 1984 September-October; 3(5): 185-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6094067

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Expression of alpha-synuclein in the human brain: relation to Lewy body disease. Author(s): Wirdefeldt K, Bogdanovic N, Westerberg L, Payami H, Schalling M, Murdoch G. Source: Brain Research. Molecular Brain Research. 2001 August 15; 92(1-2): 58-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11483242

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Familial diffuse Lewy body disease, eye movement abnormalities, and distribution of pathology. Author(s): Brett FM, Henson C, Staunton H. Source: Archives of Neurology. 2002 March; 59(3): 464-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11890854

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Familial parkinsonism, dementia, and Lewy body disease: study of family G. Author(s): Denson MA, Wszolek ZK, Pfeiffer RF, Wszolek EK, Paschall TM, McComb RD. Source: Annals of Neurology. 1997 October; 42(4): 638-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9382476

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FDG positron emission tomography in diffuse Lewy body disease: a case report. Author(s): Tatlidil R, New P, Mayberg H. Source: Clinical Nuclear Medicine. 2000 December; 25(12): 1004-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11129133

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Fluoro-deoxyglucose positron emission tomography in diffuse Lewy body disease. Author(s): Albin RL, Minoshima S, D'Amato CJ, Frey KA, Kuhl DA, Sima AA. Source: Neurology. 1996 August; 47(2): 462-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8757021

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Fluoro-DOPA and FDG positron emission tomography in a case of pathologically verified pure diffuse Lewy body disease. Author(s): Hisanaga K, Suzuki H, Tanji H, Mochizuki H, Iwasaki Y, Sato N, Jin K. Source: Journal of Neurology. 2001 October; 248(10): 905-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11697531

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Frequent coexistence of Lewy bodies and neurofibrillary tangles in the same neurons of patients with diffuse Lewy body disease. Author(s): Iseki E, Marui W, Kosaka K, Ueda K. Source: Neuroscience Letters. 1999 April 9; 265(1): 9-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10327193

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From Lewy body disease to Alzheimer's disease: hypothesis and evidence. Author(s): Wang DS. Source: Frontiers in Bioscience : a Journal and Virtual Library. 2003 May 1; 8: S223-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12700035

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Genetic polymorphism of cytochrome P450 2D6 in idiopathic Parkinson disease and diffuse Lewy body disease. Author(s): Bordet R, Broly F, Destee A, Libersa C. Source: Clinical Neuropharmacology. 1994 October; 17(5): 484-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9316701

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Glial involvement in diffuse Lewy body disease. Author(s): Terada S, Ishizu H, Yokota O, Tsuchiya K, Nakashima H, Ishihara T, Fujita D, Ueda K, Ikeda K, Kuroda S. Source: Acta Neuropathologica. 2003 February; 105(2): 163-9. Epub 2002 October 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12536227

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Glycoxidation and oxidative stress in Parkinson disease and diffuse Lewy body disease. Author(s): Castellani R, Smith MA, Richey PL, Perry G. Source: Brain Research. 1996 October 21; 737(1-2): 195-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8930366

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Hippocampal degeneration differentiates diffuse Lewy body disease (DLBD) from Alzheimer's disease: light and electron microscopic immunocytochemistry of CA2-3 neurites specific to DLBD. Author(s): Dickson DW, Ruan D, Crystal H, Mark MH, Davies P, Kress Y, Yen SH. Source: Neurology. 1991 September; 41(9): 1402-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1653914

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Hippocampal pathology in diffuse Lewy body disease using ubiquitin immunohistochemistry. Author(s): Iseki E, Li F, Odawara T, Kosaka K. Source: Journal of the Neurological Sciences. 1997 August; 149(2): 165-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9171325

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Human recombinant NACP/alpha-synuclein is aggregated and fibrillated in vitro: relevance for Lewy body disease. Author(s): Hashimoto M, Hsu LJ, Sisk A, Xia Y, Takeda A, Sundsmo M, Masliah E. Source: Brain Research. 1998 July 20; 799(2): 301-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9675319

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Image analysis of neuropil threads in Alzheimer's, Pick's, diffuse Lewy body disease and in progressive supranuclear palsy. Author(s): Davis DG, Wang HZ, Markesbery WR. Source: Journal of Neuropathology and Experimental Neurology. 1992 November; 51(6): 594-600. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1336541

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Immunohistochemistry of neuronal inclusions in the cerebral cortex and brain-stem in Lewy body disease. Author(s): Fukuda T, Tanaka J, Watabe K, Numoto RT, Minamitani M. Source: Acta Pathol Jpn. 1993 October; 43(10): 545-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8291442

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Immunoreactivity profile of hippocampal CA2/3 neurites in diffuse Lewy body disease. Author(s): Dickson DW, Schmidt ML, Lee VM, Zhao ML, Yen SH, Trojanowski JQ. Source: Acta Neuropathologica. 1994; 87(3): 269-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7912027

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Incidental Lewy body disease in a patient with REM sleep behavior disorder. Author(s): Uchiyama M, Isse K, Tanaka K, Yokota N, Hamamoto M, Aida S, Ito Y, Yoshimura M, Okawa M. Source: Neurology. 1995 April; 45(4): 709-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7723959

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Incidental Lewy body disease in black Africans. Author(s): Jendroska K, Olasode BJ, Daniel SE, Elliott L, Ogunniyi AO, Aghadiuno PU, Osuntokun BO, Lees AJ. Source: Lancet. 1994 September 24; 344(8926): 882-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7916413

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Incidental Lewy body disease. Author(s): Ben-Shlomo Y, Wenning G. Source: Lancet. 1994 November 26; 344(8935): 1503. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7968136

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Indices of oxidative stress and mitochondrial function in individuals with incidental Lewy body disease. Author(s): Dexter DT, Sian J, Rose S, Hindmarsh JG, Mann VM, Cooper JM, Wells FR, Daniel SE, Lees AJ, Schapira AH, et al. Source: Annals of Neurology. 1994 January; 35(1): 38-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8285590

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Intraneuronal Lewy body inclusions in Parkinson and diffuse Lewy body disease. Author(s): Bogdanovic N. Source: Journal of Cellular and Molecular Medicine. 2001 July-September; 5(3): 318-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12067491

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Is there apoptosis in Lewy body disease? Author(s): Jellinger KA. Source: Acta Neuropathologica. 1999 April; 97(4): 413-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10208282

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Isofurans, but not F2-isoprostanes, are increased in the substantia nigra of patients with Parkinson's disease and with dementia with Lewy body disease. Author(s): Fessel JP, Hulette C, Powell S, Roberts LJ 2nd, Zhang J. Source: Journal of Neurochemistry. 2003 May; 85(3): 645-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12694390

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Levodopa improved rapid eye movement sleep behavior disorder with diffuse Lewy body disease. Author(s): Yamauchi K, Takehisa M, Tsuno M, Kaneda Y, Taniguchi T, Ohno H, Sei H, Morita Y, Ohmori T. Source: General Hospital Psychiatry. 2003 March-April; 25(2): 140-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12676431

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Lewy bodies are located preferentially in limbic areas in diffuse Lewy body disease. Author(s): Rezaie P, Cairns NJ, Chadwick A, Lantos PL. Source: Neuroscience Letters. 1996 July 12; 212(2): 111-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8832651

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Lewy bodies: purification from diffuse Lewy body disease brains. Author(s): Iwatsubo T, Yamaguchi H, Fujimuro M, Yokosawa H, Ihara Y, Trojanowski JQ, Lee VM. Source: Annals of the New York Academy of Sciences. 1996 June 15; 786: 195-205. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8687019

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Lewy body disease and dementia. A review. Author(s): Kalra S, Bergeron C, Lang AE. Source: Archives of Internal Medicine. 1996 March 11; 156(5): 487-93. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8604954

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Lewy body disease in a patient with REM sleep disorder. Author(s): Negro PJ Jr, Faber R. Source: Neurology. 1996 May; 46(5): 1493-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8628517

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Lewy body disease with and without dementia: a clinicopathological study of 35 cases. Author(s): Kosaka K, Tsuchiya K, Yoshimura M. Source: Clin Neuropathol. 1988 November-December; 7(6): 299-305. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3224472

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Lewy body disease. Author(s): Riley DE. Source: Archives of Neurology. 2002 June; 59(6): 1043; Author Reply 1043-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12056948

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Lewy body disease. Author(s): Smith TA, Prayson RA. Source: Southern Medical Journal. 1996 December; 89(12): 1174-80. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8969351

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Lewy body disease. Author(s): Hansen LA, Galasko D. Source: Curr Opin Neurol Neurosurg. 1992 December; 5(6): 889-94. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1467583

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Lewy body disease. Author(s): Gibb WR, Lees AJ. Source: Neurology. 1989 June; 39(6): 878-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2725899

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Lewy body disease: can we diagnose it? Author(s): Papka M, Rubio A, Schiffer RB, Cox C. Source: The Journal of Neuropsychiatry and Clinical Neurosciences. 1998 Fall; 10(4): 405-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9813785

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Meige syndrome in the spectrum of Lewy body disease. Author(s): Mark MH, Sage JI, Dickson DW, Heikkila RE, Manzino L, Schwarz KO, Duvoisin RC. Source: Neurology. 1994 August; 44(8): 1432-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8058144

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Morphological substrates of mental dysfunction in Lewy body disease: an update. Author(s): Jellinger KA. Source: Journal of Neural Transmission. Supplementum. 2000; 59: 185-212. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10961431

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Multicatalytic proteinase is present in Lewy bodies and neurofibrillary tangles in diffuse Lewy body disease brains. Author(s): Kwak S, Masaki T, Ishiura S, Sugita H. Source: Neuroscience Letters. 1991 July 8; 128(1): 21-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1656333

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Neuroaxonal dystrophy combined with diffuse Lewy body disease in a young adult. Author(s): Sugiyama H, Hainfellner JA, Schmid-Siegel B, Budka H. Source: Clin Neuropathol. 1993 May-June; 12(3): 147-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8391956

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Neurofibrillary tangles in the dentate granule cells of patients with Alzheimer's disease, Lewy body disease and progressive supranuclear palsy. Author(s): Wakabayashi K, Hansen LA, Vincent I, Mallory M, Masliah E. Source: Acta Neuropathologica. 1997 January; 93(1): 7-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9006651

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Neuropathological diagnoses in elderly patients in Oslo: Alzheimer's disease, Lewy body disease, vascular lesions. Author(s): Ince PG, McArthur FK, Bjertness E, Torvik A, Candy JM, Edwardson JA. Source: Dementia. 1995 May-June; 6(3): 162-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7620529

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Neuropathological evaluation and apolipoprotein E gene polymorphism analysis in diffuse Lewy body disease. Author(s): Kawanishi C, Suzuki K, Odawara T, Iseki E, Onishi H, Miyakawa T, Yamada Y, Kosaka K, Kondo N, Yamamoto T. Source: Journal of the Neurological Sciences. 1996 March; 136(1-2): 140-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8815160

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Neuropsychiatric features of Lewy body disease. Author(s): Filley CM. Source: Brain and Cognition. 1995 August; 28(3): 229-39. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8546851

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Neuropsychiatric manifestations of diffuse Lewy body disease. Author(s): Beck BJ. Source: Journal of Geriatric Psychiatry and Neurology. 1995 July; 8(3): 189-96. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7576045

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Neuropsychological deficits associated with diffuse Lewy body disease. Author(s): Salmon DP, Galasko D, Hansen LA, Masliah E, Butters N, Thal LJ, Katzman R. Source: Brain and Cognition. 1996 July; 31(2): 148-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8811990

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Nigral and cortical Lewy bodies and dystrophic nigral neurites in Parkinson's disease and cortical Lewy body disease contain alpha-synuclein immunoreactivity. Author(s): Irizarry MC, Growdon W, Gomez-Isla T, Newell K, George JM, Clayton DF, Hyman BT. Source: Journal of Neuropathology and Experimental Neurology. 1998 April; 57(4): 3347. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9600226

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Odor identification deficits in diffuse lewy body disease. Author(s): Westervelt HJ, Stern RA, Tremont G. Source: Cognitive and Behavioral Neurology : Official Journal of the Society for Behavioral and Cognitive Neurology. 2003 June; 16(2): 93-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12799595

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Oxidative stress as a cause of nigral cell death in Parkinson's disease and incidental Lewy body disease. The Royal Kings and Queens Parkinson's Disease Research Group. Author(s): Jenner P, Dexter DT, Sian J, Schapira AH, Marsden CD. Source: Annals of Neurology. 1992; 32 Suppl: S82-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1510385

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Parkinsonian features of eight pathologically diagnosed cases of diffuse Lewy body disease. Author(s): Louis ED, Goldman JE, Powers JM, Fahn S. Source: Movement Disorders : Official Journal of the Movement Disorder Society. 1995 March; 10(2): 188-94. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7753061

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Pathologically diagnosed diffuse Lewy body disease and Parkinson's disease. Do the parkinsonian features differ? Author(s): Louis ED, Fahn S. Source: Adv Neurol. 1996; 69: 311-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8615144

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Probable diffuse Lewy body disease presenting as REM sleep behavior disorder. Author(s): Turner RS, Chervin RD, Frey KA, Minoshima S, Kuhl DE. Source: Neurology. 1997 August; 49(2): 523-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9270589

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Production of anti-polyubiquitin and anti-ubiquitin carboxyl terminal hydrolase antibodies and immunohistochemically assessment of them on brain sections of Alzheimer's disease and Lewy body disease. Author(s): Pirim I. Source: The International Journal of Neuroscience. 1998 July; 95(1-2): 33-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9845014

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Psychiatric features in diffuse Lewy body disease. Author(s): Ballard C, McKeith IG. Source: Neurology. 1998 February; 50(2): 573. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9484409

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Psychiatric features in diffuse Lewy body disease: a clinicopathologic study using Alzheimer's disease and Parkinson's disease comparison groups. Author(s): Klatka LA, Louis ED, Schiffer RB. Source: Neurology. 1996 November; 47(5): 1148-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8909420

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Purification and characterization of Lewy bodies from the brains of patients with diffuse Lewy body disease. Author(s): Iwatsubo T, Yamaguchi H, Fujimuro M, Yokosawa H, Ihara Y, Trojanowski JQ, Lee VM. Source: American Journal of Pathology. 1996 May; 148(5): 1517-29. Erratum In: Am J Pathol 1996 November; 149(5): 1770-1. Am J Pathol 1997 June; 150(6): 2255. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8623921

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Regional brain atrophy in idiopathic parkinson's disease and diffuse Lewy body disease. Author(s): Double KL, Halliday GM, McRitchie DA, Reid WG, Hely MA, Morris JG. Source: Dementia. 1996 November-December; 7(6): 304-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8915036

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Regional brain atrophy in progressive supranuclear palsy and Lewy body disease. Author(s): Cordato NJ, Halliday GM, Harding AJ, Hely MA, Morris JG. Source: Annals of Neurology. 2000 June; 47(6): 718-28. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10852537

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REM sleep behavior disorder and degenerative dementia: an association likely reflecting Lewy body disease. Author(s): Boeve BF, Silber MH, Ferman TJ, Kokmen E, Smith GE, Ivnik RJ, Parisi JE, Olson EJ, Petersen RC. Source: Neurology. 1998 August; 51(2): 363-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9710004

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Role of cytochrome c as a stimulator of alpha-synuclein aggregation in Lewy body disease. Author(s): Hashimoto M, Takeda A, Hsu LJ, Takenouchi T, Masliah E. Source: The Journal of Biological Chemistry. 1999 October 8; 274(41): 28849-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10506125

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Senile dementia of Lewy body type and spectrum of Lewy body disease. Author(s): Perry RH, Irving D, Blessed G, Perry EK, Fairbairn AF. Source: Lancet. 1989 May 13; 1(8646): 1088. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2566043

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Serum levels of coenzyme Q in patients with Lewy body disease. Author(s): Molina JA, de Bustos F, Ortiz S, Del Ser T, Seijo M, Benito-Leon J, Oliva JM, Perez S, Manzanares J. Source: Journal of Neural Transmission (Vienna, Austria : 1996). 2002 September; 109(9): 1195-201. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12203046

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Synapse alterations in the hippocampal-entorhinal formation in Alzheimer's disease with and without Lewy body disease. Author(s): Wakabayashi K, Honer WG, Masliah E. Source: Brain Research. 1994 December 19; 667(1): 24-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7895080

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Temporal pattern of cognitive decline and incontinence is different in Alzheimer's disease and diffuse Lewy body disease. Author(s): Del-Ser T, Munoz DG, Hachinski V. Source: Neurology. 1996 March; 46(3): 682-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8618667

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The clinicopathologic spectrum of Lewy body disease. Author(s): Mark MH, Dickson DW, Sage JI, Duvoisin RC. Source: Adv Neurol. 1996; 69: 315-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8615145

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The evolution of cerebral perfusion abnormalities in Lewy body disease: assessment with Tc-99m hexamethylpropylene amineoxime single photon emission computed tomography. Author(s): Lorberboym M, Lampl Y. Source: Semin Nucl Med. 2001 April; 31(2): 165-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11330787

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The presence of tau distinguishes Lewy bodies of diffuse Lewy body disease from those of idiopathic Parkinson disease. Author(s): Galloway PG, Bergeron C, Perry G. Source: Neuroscience Letters. 1989 May 22; 100(1-3): 6-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2548130

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The relationship between Lewy body disease, Parkinson's disease, and Alzheimer's disease. Author(s): Hardy J. Source: Annals of the New York Academy of Sciences. 2003 June; 991: 167-70. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12846985

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The topographic distribution of brain atrophy in cortical Lewy body disease: comparison with Alzheimer's disease. Author(s): Mann DM, Snowden JS. Source: Acta Neuropathologica. 1995; 89(2): 178-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7732790

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Upregulation of the anti-apoptotic protein Bcl-2 may be an early event in neurodegeneration: studies on Parkinson's and incidental Lewy body disease. Author(s): Marshall KA, Daniel SE, Cairns N, Jenner P, Halliwell B. Source: Biochemical and Biophysical Research Communications. 1997 November 7; 240(1): 84-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9367887

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Visual hallucinations in Lewy body disease relate to Lewy bodies in the temporal lobe. Author(s): Harding AJ, Broe GA, Halliday GM. Source: Brain; a Journal of Neurology. 2002 February; 125(Pt 2): 391-403. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11844739

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What are the relations between Lewy body disease and AD? Author(s): McKeith IG, Ince P, Jaros EB, Fairbairn A, Ballard C, Grace J, Morris CM, Perry RH. Source: Journal of Neural Transmission. Supplementum. 1998; 54: 107-16. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9850919

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CHAPTER 2. PATENTS ON LEWY BODY DISEASE Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.7 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “Lewy body disease” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on Lewy body disease, we have not necessarily excluded non-medical patents in this bibliography.

Patent Applications on Lewy Body Disease As of December 2000, U.S. patent applications are open to public viewing.8 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to Lewy body disease:

7Adapted

from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm. 8 This has been a common practice outside the United States prior to December 2000.

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Development of transgenic model for interventions in neurodegenerative diseases Inventor(s): Mallory, Margaret E.; (Encinitas, CA), Masliah, Eliezer; (San Diego, CA), Rockenstein, Edward; (Chula Vista, CA) Correspondence: Brown, Martin, Haller & Mcclain Llp; 1660 Union Street; San Diego; CA; 92101-2926; US Patent Application Number: 20030056231 Date filed: August 20, 2001 Abstract: Alzheimer's disease, Parkinson's disease and Lewy body disease are the most commonly found neurodegenerative disorders in the elderly. The invention is a transgenic mouse that contains two transgenes, human.alpha.-synuclein and human amyloid precursor protein, which are responsible for the formation of the neuritic plaques, Lewy bodies and neurodegeneration seen in the above mentioned diseases. The transgenic mouse is an accurate model for disease by both functional and pathological assays. Excerpt(s): This invention relates to transgenic mice for use in the study of neurodegenerative diseases. Alzheimer's disease (AD), Parkinson's disease (PD) and Lewy Body disease (LBD) are the most commonly found neurodegenerative disorders in the elderly. Although their incidence continues to increase, creating a serious public health problem, to date these disorders are neither curable nor preventable. There is a genetic component to these diseases, however most cases arise spontaneously in the population in the absence of mutations. Nerve damage results from the development of protein aggregates composed of proteins normally expressed in the brain. It is not known what causes the conversion of normally non-toxic proteins to their toxic state. Recent epidemiological studies have demonstrated a close clinical relationship between AD and PD, as about 30% of Alzheimer's patients also have PD. Compared to the rest of the aging population, patients with AD are more likely to develop concomitant PD. Furthermore, PD patients that become demented usually have developed classical AD. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Polyhydroxylated aromatic compounds for the treatment of amyloidosis and alphasynuclein fibril diseases Inventor(s): Castillo, Gerardo M.; (Seattle, WA), Choi, Paula Y.; (Bothell, WA), Snow, Alan D.; (Lynnwood, WA) Correspondence: Heller Ehrman White & Mcauliffe Llp; 275 Middlefield Road; Menlo Park; CA; 94025-3506; US Patent Application Number: 20010047032 Date filed: December 26, 2000 Abstract: Polyhydroxylated aromatic compounds, and compositions containing them, are useful for the treatment of amyloidosis, especially Alzheimer's disease, and for the treatment of diseases characterized by.alpha.-synuclein fibril formation, especially Lewy body disease and Parkinson's disease. Excerpt(s): This invention relates to the use of certain polyhydroxylated aromatic compounds, and compositions containing them, for the treatment of amyloidosis, especially Alzheimer's disease, and the treatment of diseases characterized by.alpha.synuclein fibril formation, especially Lewy body disease and Parkinson's disease.

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Amyloid is a generic term referring to a group of diverse but specific extracellular protein deposits which all have common morphological properties, staining characteristics, and X-ray diffraction spectra. Regardless of the nature of the amyloid protein deposited all amyloids have the following characteristics: 1) showing an amorphous appearance at the light microscopic level, appearing eosinophilic using hematoxylin and eosin stains; 2) staining with Congo red and demonstrating a red/green birefringence as viewed under polarized light (Puchtler et al., J. Histochem. Cytochem. 10:355-364, 1962), 3) containing a predominant beta-pleated sheet secondary structure, and 4) ultrastructurally consisting of non-branching fibrils of indefinite length and with a diameter of 7-10 nm. Amyloidoses today are classified according to the specific amyloid protein deposited. The amyloids include, but are not limited to, the amyloid associated with Alzheimer's disease, Down's syndrome and hereditary cerebral hemorrhage with amyloidosis of the Dutch type (where the specific amyloid is referred to as beta-amyloid protein or A.beta.), the amyloid associated with chronic inflammation, various forms of malignancy and familial Mediterranean fever (where the specific amyloid is referred to as AA amyloid or inflammation-associated amyloid), the amyloid associated with multiple myeloma and other B-cell dyscrasias (where the specific amyloid is referred to as AL amyloid), the amyloid associated with type II diabetes (where the specific amyloid is referred to as amylin or islet amyloid), the amyloid associated with the prion diseases including Creutzfeldt-Jakob disease, Gerstmann-Straussler syndrome, kuru, and scrapie (where the specific amnyloid is referred to as PrP amyloid), the amyloid associated with long-term hemodialysis and carpal tunnel syndrome (where the specific amyloid is referred to as beta.sub.2microglobulin amyloid), the amyloid associated with senile cardiac amyloid and familial amyloidotic polyneuropathy (where the specific amyloid is referred to as prealbumin or transthyretin amyloid), and the amyloid associated with endocrine tumors such as medullary carcinoma of the thyroid (where the specific amyloid is referred to as variants of procalcitonin). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Keeping Current In order to stay informed about patents and patent applications dealing with Lewy body disease, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “Lewy body disease” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on Lewy body disease. You can also use this procedure to view pending patent applications concerning Lewy body disease. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 3. BOOKS ON LEWY BODY DISEASE Overview This chapter provides bibliographic book references relating to Lewy body disease. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on Lewy body disease include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.

Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “Lewy body disease” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on Lewy body disease: •

Dementia With Lewy Bodies: Clinical, Pathological, and Treatment Issues Source: New York, NY: Cambridge University Press. 1996. 510 p. Contact: Available from Cambridge University Press. 110 Midland Avenue, Port Chester, NY 10573-4930. (800) 872-7423; (914) 937-9600; FAX (914) 937-4712. PRICE: $125.00. ISBN: 0521561884. Summary: This book discusses the clinical aspects, neuropathology, and treatment of dementia with Lewy bodies (DLB). It includes review articles, case studies, and recent research findings from the main centers studying DLB. The purpose of the book is to establish clinical diagnostic criteria and pathological protocols for DLB, and to explore evidence suggesting that patients with DLB may be responsive to symptomatic treatment. The first section, on clinical issues, discusses the clinical diagnosis of DLB, the differentiation of DLB from dementias of other etiologies, cognitive and noncognitive

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symptoms, the neuroanatomical basis of cognitive symptoms, and functional imaging findings in DLB and related dementias. The second part, on pathological issues, discusses the neuropathological features of DLB and other Lewy body diseases, the relationship of DLB to Alzheimer's disease and Parkinson's disease, the pathogenesis of the Lewy body, and genetic aspects of DLB. The third part, on treatment issues, addresses the neurochemistry of DLB, the management of noncognitive symptoms, cholinergic therapy, and other pharmacological strategies. Appendices contain guidelines for the clinical diagnosis and neuropathological evaluation of DLB. •

Ageing, Neuropsychology and the 'New' Dementias: Definitions, Explanations and Practical Approaches Source: San Diego, CA: Singular Publishing Group, Inc. 1995. 157 p. Contact: Singular Publishing Group, Inc. 4284 41st Street, San Diego, CA 92105-1197. (800) 521-8545; FAX (800) 774-8398. PRICE: $42.99. ISBN: 0412613409. Summary: This book is designed to introduce health professionals to current concepts in neuropsychology, behavior, and dementia in older people. It is intended to clarify some of the existing terminology, describe a realistic approach to neuropsychological assessment, and offer practical solutions to common problems encountered in the older population. It discusses issues in interpreting behaviors, recognizing problems, and preparing older people for assessment. It describes basic neuropsychological investigations; explores a new approach to the concept of dementia; and reviews some of the newly identified dementias including the AIDS dementia complex, Lewy body disease, and human prion disease. Other topics include head injury in older people, rehabilitation and retraining, and community care. Appendices contain definitions of terms, hyperventilation guidelines, and suggested guidelines for communication difficulties.

Chapters on Lewy Body Disease In order to find chapters that specifically relate to Lewy body disease, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and Lewy body disease using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “Lewy body disease” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on Lewy body disease: •

Memory Impairments Underlying Language Difficulties in Dementia Source: in Gillam, R.B., ed. Memory and Language Impairment in Children and Adults: New Perspectives. Gaithersburg, MD: Aspen Publishers, Inc. 1998. p. 191-208. Contact: Available from Aspen Publishers, Inc. 200 Orchard Ridge Drive, Suite 200, Gaithersburg, MD 20878. (800) 638-8437. Website: www.aspenpublishers.com. PRICE: $35.00. ISBN: 0834212137. Summary: Difficulties with storing, retaining, recalling, and reporting information places individuals with language impairments at a significant disadvantage in academic, vocational, and social situations. This chapter on memory impairments

Books

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underlying language difficulties is from a textbook that discusses language assessment and intervention strategies that take into account how cognitive systems such as memory contribute to learning and using language. In this chapter, the authors describe the memory profiles of patients with different dementia producing diseases, the impact of memory deficits on language, some of the individual tests and test batteries used to assess memory and language impairments, and several strategies for facilitating language in dementia patients. The scope of the chapter is limited to a discussion of Alzheimer's disease (AD), the most common of the cortical dementias; Parkinson's disease (PD), the most common of the subcortical dementias; and Lewy body disease (LBD), which typically results in both cortical and subcortical neuropathology. Individuals with dementia display progressive impairments in semantic, episodic, and lexical memory. Dementia also results in working memory limitations. The authors stress that understanding the patterns of impaired and preserved memory functions in dementia patients and their impact on communicative ability can lead to the development of more effective assessment techniques and clinical interventions. The most effective strategies for facilitating language comprehension and production in dementia patients are those that minimize attentional, working, and declarative memory demands. 2 tables. 66 references.

45

APPENDICES

47

APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.

NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute9: •

Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm

•

National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/

•

National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html

•

National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25

•

National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm

•

National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm

•

National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375

•

National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/

9

These publications are typically written by one or more of the various NIH Institutes.

48

Lewy Body Disease

•

National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm

•

National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

•

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

•

National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

•

National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

•

National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

•

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm

•

National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html

•

National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

•

National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

•

National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm

•

National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html

•

National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

•

Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

•

National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

•

National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp

•

Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html

•

Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm

Physician Resources

49

NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.10 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:11 •

Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html

•

HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html

•

NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html

•

Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/

•

Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html

•

Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html

•

Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/

•

Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html

•

Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html

•

Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html

•

MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html

10

Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 11 See http://www.nlm.nih.gov/databases/databases.html.

50

Lewy Body Disease

•

Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html

•

Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html

The NLM Gateway12 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.13 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “Lewy body disease” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total

Items Found 904 1 305 0 18 1228

HSTAT14 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.15 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.16 Simply search by “Lewy body disease” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

12

Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

13

The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 14 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 15 16

The HSTAT URL is http://hstat.nlm.nih.gov/.

Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.

Physician Resources

51

Coffee Break: Tutorials for Biologists17 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.18 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.19 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.

Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •

CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.

•

Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.

17 Adapted 18

from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.

The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 19 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.

53

APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on Lewy body disease can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internetbased services that post them.

Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to Lewy body disease. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to Lewy body disease. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “Lewy body disease”:

54

Lewy Body Disease

Alzheimer's Disease http://www.nlm.nih.gov/medlineplus/alzheimersdisease.html Degenerative Nerve Diseases http://www.nlm.nih.gov/medlineplus/degenerativenervediseases.html Dementia http://www.nlm.nih.gov/medlineplus/dementia.html Huntington's Disease http://www.nlm.nih.gov/medlineplus/huntingtonsdisease.html Parkinson's Disease http://www.nlm.nih.gov/medlineplus/parkinsonsdisease.html You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on Lewy body disease. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •

Dementias Source: NSW, Australia: Alzheimer's Association NSW. 1997. 5 p. Contact: Available from Alzheimer's Association NSW. PO Box 6042, North Ryde, NSW, 1670 Australia. Internet: http://www.alznsw.asn.au. PRICE: Download free from Internet. Summary: This fact sheet describes the different types of dementias. Dementia is a term used for loss of mental function that affects daily life. The most common forms of dementia are Alzheimer's disease, Parkinson's disease, Diffuse Lewy Body disease, and vascular dementia. Frontal lobe or fronto-temporal dementias include Pick's disease and Huntington's disease. Excess use of alcohol can lead to Korsakoff's dementia. Structural brain problems such as head injury, benign tumors or hydrocephalus can also lead to dementia. Some forms of dementia are due to infection or Cruezfeldt Jakob disease. Dementia-like symptoms that are treatable or potentially reversible can come from medical conditions such as vitamin or hormonal deficiencies, medication interactions, or psychiatric disorders.

Patient Resources

•

55

Overview of Alzheimer's Disease and Related Dementias Source: Alzheimer's Association. 919 Michigan Avenue, Suite 1000, Chicago, IL 606111676. (800)272-3900; TDD (312)335-8882. Internet access: http://www.alz.org. PRICE: Free. Order Number ED205Z. Summary: This pamphlet distributed by the Alzheimer's Association provides a comprehensive overview of Alzheimer's disease (AD). It covers several AD-related topics, including causes, familial risk, age of onset, diagnosis, treatment, differences between AD and normal age-related memory difficulties, memory loss as a natural part of aging, and other dementia-causing conditions. These conditions include CreutzfeldtJakob disease, normal pressure hydrocephalus, Pick's disease, Parkinson's disease, Lewy body disease, Huntington's disease, and depression. A list of services and resource materials available through the Alzheimer's Association is provided. 1 figure, 1 table, illustration. The NIH Search Utility

The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to Lewy body disease. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats

•

Family Village: http://www.familyvillage.wisc.edu/specific.htm

•

Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/

•

Med Help International: http://www.medhelp.org/HealthTopics/A.html

•

Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/

•

Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/

•

WebMDHealth: http://my.webmd.com/health_topics

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to Lewy body disease. By consulting all of associations

56

Lewy Body Disease

listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with Lewy body disease. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about Lewy body disease. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “Lewy body disease” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “Lewy body disease”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “Lewy body disease” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “Lewy body disease” (or a synonym) into the search box, and click “Submit Query.”

57

APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.

Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.20

Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.

Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of

20

Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.

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Lewy Body Disease

libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)21: •

Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/

•

Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)

•

Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm

•

California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html

•

California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html

•

California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html

•

California: Gateway Health Library (Sutter Gould Medical Foundation)

•

California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/

•

California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp

•

California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html

•

California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/

•

California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/

•

California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/

•

California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html

•

California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/

•

Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/

•

Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/

•

Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/

21

Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.

Finding Medical Libraries

59

•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

•

Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm

•

Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html

•

Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm

•

Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp

•

Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/

•

Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm

•

Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html

•

Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/

•

Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm

•

Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/

•

Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/

•

Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/

•

Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm

•

Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html

•

Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm

•

Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/

•

Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/

•

Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10

•

Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/

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•

Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html

•

Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp

•

Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp

•

Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/

•

Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

•

Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

•

Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

•

Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

•

Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

•

Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

•

Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

•

Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

•

Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

•

Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm

•

Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330

•

Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

•

National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

•

National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/

•

National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

Finding Medical Libraries

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•

Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm

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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/

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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •

ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html

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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp

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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/

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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html

•

On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/

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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp

•

Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm

Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).

Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •

Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical

•

MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

•

Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

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LEWY BODY DISEASE DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine: A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acidity: The quality of being acid or sour; containing acid (hydrogen ions). [EU] Actin: Essential component of the cell skeleton. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized

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amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Angiopathy: Disease of the blood vessels (arteries, veins, and capillaries) that occurs when someone has diabetes for a long time. There are two types of angiopathy: macroangiopathy and microangiopathy. In macroangiopathy, fat and blood clots build up in the large blood vessels, stick to the vessel walls, and block the flow of blood. In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body. Then the cells, for example, the ones in the center of the eye, do not get enough blood and may be damaged. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Ansa: A turn or bend in a thread or line; a bend in a wire; one of the patterns formed by the dermal ridges on the finger tips. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]

Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are

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highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autopsy: Postmortem examination of the body. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Benign tumor: A noncancerous growth that does not invade nearby tissue or spread to other parts of the body. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [NIH]

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Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [NIH] Bipolar Disorder: A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence. [NIH] Bladder: The organ that stores urine. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]

Cardiac: Having to do with the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Carpal Tunnel Syndrome: A median nerve injury inside the carpal tunnel that results in symptoms of pain, numbness, tingling, clumsiness, and a lack of sweating, which can be caused by work with certain hand and wrist postures. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH]

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Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebellar Diseases: Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, gait ataxia, and muscle hypotonia. [NIH] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebral Hemorrhage: Bleeding into a cerebral hemisphere of the brain, including lobar, subcortical white matter, and basal ganglia hemorrhages. Commonly associated conditions include hypertension; intracranial arteriosclerosis; intracranial aneurysm; craniocerebral trauma; intracranial arteriovenous malformations; cerebral amyloid angiopathy; and cerebral infarction. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Circadian: Repeated more or less daily, i. e. on a 23- to 25-hour cycle. [NIH]

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Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]

Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body,

Dictionary 71

taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Concomitant: Accompanying; accessory; joined with another. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Criterion: A standard by which something may be judged. [EU] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or

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involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delusions: A false belief regarding the self or persons or objects outside the self that persists despite the facts, and is not considered tenable by one's associates. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH] Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Dissociative Disorders: Sudden temporary alterations in the normally integrative functions of consciousness. [NIH] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Dopa: The racemic or DL form of DOPA, an amino acid found in various legumes. The

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dextro form has little physiologic activity but the levo form (levodopa) is a very important physiologic mediator and precursor and pharmacological agent. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dystrophic: Pertaining to toxic habitats low in nutrients. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]

Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used for the broader group. [NIH] Enkephalins: One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla. [NIH] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]

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Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Estrogen: One of the two female sex hormones. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extrapyramidal: Outside of the pyramidal tracts. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Feasibility Studies: Studies to determine the advantages or disadvantages, practicability, or capability of accomplishing a projected plan, study, or project. [NIH] Fibril: Most bacterial viruses have a hollow tail with specialized fibrils at its tip. The tail fibers attach to the cell wall of the host. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Fourth Ventricle: An irregularly shaped cavity in the rhombencephalon, between the medulla oblongata, the pons, and the isthmus in front, and the cerebellum behind. It is continuous with the central canal of the cord below and with the cerebral aqueduct above, and through its lateral and median apertures it communicates with the subarachnoid space. [NIH]

Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Gait: Manner or style of walking. [NIH]

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Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Globus Pallidus: The representation of the phylogenetically oldest part of the corpus striatum called the paleostriatum. It forms the smaller, more medial part of the lentiform nucleus. [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]

Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Granule: A small pill made from sucrose. [EU] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Hematoxylin: A dye obtained from the heartwood of logwood (Haematoxylon campechianum Linn., Leguminosae) used as a stain in microscopy and in the manufacture of ink. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid.

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The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]

Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hydrocephalus: Excessive accumulation of cerebrospinal fluid within the cranium which may be associated with dilation of cerebral ventricles, intracranial hypertension; headache; lethargy; urinary incontinence; and ataxia (and in infants macrocephaly). This condition may be caused by obstruction of cerebrospinal fluid pathways due to neurologic abnormalities, intracranial hemorrhages; central nervous system infections; brain neoplasms; craniocerebral trauma; and other conditions. Impaired resorption of cerebrospinal fluid from the arachnoid villi results in a communicating form of hydrocephalus. Hydrocephalus ex-vacuo refers to ventricular dilation that occurs as a result of brain substance loss from cerebral infarction and other conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperventilation: A pulmonary ventilation rate faster than is metabolically necessary for the exchange of gases. It is the result of an increased frequency of breathing, an increased tidal volume, or a combination of both. It causes an excess intake of oxygen and the blowing off of carbon dioxide. [NIH] Hypokinesia: Slow or diminished movement of body musculature. It may be associated

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with basal ganglia diseases; mental disorders; prolonged inactivity due to illness; experimental protocols used to evaluate the physiologic effects of immobility; and other conditions. [NIH] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Illusions: The misinterpretation of a real external, sensory experience. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incidental: 1. Small and relatively unimportant, minor; 2. Accompanying, but not a major part of something; 3. (To something) Liable to occur because of something or in connection with something (said of risks, responsibilities, .) [EU] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]

Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Inotropic: Affecting the force or energy of muscular contractions. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix

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glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] Intermediate Filaments: Cytoplasmic filaments intermediate in diameter (about 10 nanometers) between the microfilaments and the microtubules. They may be composed of any of a number of different proteins and form a ring around the cell nucleus. [NIH] Intracellular: Inside a cell. [NIH] Intracranial Aneurysm: A saclike dilatation of the walls of a blood vessel, usually an artery. [NIH]

Intracranial Arteriosclerosis: Vascular diseases characterized by thickening, hardening, and remodeling of the walls of intracranial arteries. There are three subtypes: (1) atherosclerosis, marked by fatty depositions in the innermost layer of the arterial walls, (2) Monckeberg's sclerosis, which features calcium deposition in the media and (3) arteriolosclerosis, which refers to sclerosis of small caliber arteries. Clinically, this process may be associated with transient ischemic attack, brain infarction, intracranial embolism and thrombosis, or intracranial aneurysm. [NIH] Intracranial Hemorrhages: Bleeding within the intracranial cavity, including hemorrhages in the brain and within the cranial epidural, subdural, and subarachnoid spaces. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Islet: Cell producing insulin in pancreas. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Levo: It is an experimental treatment for heroin addiction that was developed by German scientists around 1948 as an analgesic. Like methadone, it binds with opioid receptors, but it is longer acting. [NIH] Levodopa: The naturally occurring form of dopa and the immediate precursor of dopamine. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. It is used for the treatment of parkinsonism and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system. [NIH]

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Ligands: A RNA simulation method developed by the MIT. [NIH] Limbic: Pertaining to a limbus, or margin; forming a border around. [EU] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Locomotor: Of or pertaining to locomotion; pertaining to or affecting the locomotive apparatus of the body. [EU] Locus Coeruleus: Bluish region in the superior angle of the fourth ventricle floor, corresponding to melanin-like pigmented nerve cells which lie lateral to the pontomesencephalic central gray (griseum centrale). It is also known as nucleus pigmentosus pontis. [NIH] Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Manic: Affected with mania. [EU] Median Nerve: A major nerve of the upper extremity. In humans, the fibers of the median nerve originate in the lower cervical and upper thoracic spinal cord (usually C6 to T1), travel via the brachial plexus, and supply sensory and motor innervation to parts of the forearm and hand. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU]

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Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Megalencephaly: A condition in which there is an abnormally large, heavy, and usually malfunctioning brain. [NIH] Melanin: The substance that gives the skin its color. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mesencephalic: Ipsilateral oculomotor paralysis and contralateral tremor, spasm. or choreic movements of the face and limbs. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microtubule-Associated Proteins: High molecular weight proteins found in the microtubules of the cytoskeletal system. Under certain conditions they are required for tubulin assembly into the microtubules and stabilize the assembled microtubules. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Motility: The ability to move spontaneously. [EU]

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Motor nerve: An efferent nerve conveying an impulse that excites muscular contraction. [NIH]

Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Neocortex: The largest portion of the cerebral cortex. It is composed of neurons arranged in six layers. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurites: In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell. [NIH] Neurodegenerative Diseases: Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures. [NIH] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [NIH] Neurofibrillary Tangles: Abnormal structures located in various parts of the brain and composed of dense arrays of paired helical filaments (neurofilaments and microtubules). These double helical stacks of transverse subunits are twisted into left-handed ribbon-like filaments that likely incorporate the following proteins: (1) the intermediate filaments: medium- and high-molecular-weight neurofilaments; (2) the microtubule-associated proteins map-2 and tau; (3) actin; and (4) ubiquitin. As one of the hallmarks of Alzheimer disease, the neurofibrillary tangles eventually occupy the whole of the cytoplasm in certain classes of cell in the neocortex, hippocampus, brain stem, and diencephalon. The number of these tangles, as seen in post mortem histology, correlates with the degree of dementia during life. Some studies suggest that tangle antigens leak into the systemic circulation both in the course of normal aging and in cases of Alzheimer disease. [NIH] Neurofilaments: Bundle of neuronal fibers. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU]

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Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neuronal Plasticity: The capacity of the nervous system to change its reactivity as the result of successive activations. [NIH] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropil: A dense intricate feltwork of interwoven fine glial processes, fibrils, synaptic terminals, axons, and dendrites interspersed among the nerve cells in the gray matter of the central nervous system. [NIH] Neuropil Threads: Abnormal structures located chiefly in distal dendrites and, along with neurofibrillary tangles and senile plaques, constitute the three morphological hallmarks of Alzheimer disease. Neuropil threads are made up of straight and paired helical filaments which consist of abnormally phosphorylated microtubule-associated tau proteins. It has been suggested that the threads have a major role in the cognitive impairment seen in Alzheimer disease. [NIH] Neuropsychology: A branch of psychology which investigates the correlation between experience or behavior and the basic neurophysiological processes. The term neuropsychology stresses the dominant role of the nervous system. It is a more narrowly defined field than physiological psychology or psychophysiology. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Oculomotor: Cranial nerve III. It originate from the lower ventral surface of the midbrain and is classified as a motor nerve. [NIH] Olfaction: Function of the olfactory apparatus to perceive and discriminate between the molecules that reach it, in gas form from an external environment, directly or indirectly via

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the nose. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]

Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]

Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parietal Lobe: Upper central part of the cerebral hemisphere. [NIH] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Particle: A tiny mass of material. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]

Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic

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nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]

Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Pons: The part of the central nervous system lying between the medulla oblongata and the mesencephalon, ventral to the cerebellum, and consisting of a pars dorsalis and a pars ventralis. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postural: Pertaining to posture or position. [EU] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Prealbumin: A tetrameric protein, molecular weight between 50,000 and 70,000, consisting of 4 equal chains, and migrating on electrophoresis in 3 fractions more mobile than serum albumin. Its concentration ranges from 7 to 33 per cent in the serum, but levels decrease in liver disease. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU]

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Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prion: Small proteinaceous infectious particles that resist inactivation by procedures modifying nucleic acids and contain an abnormal isoform of a cellular protein which is a major and necessary component. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Pruritus: An intense itching sensation that produces the urge to rub or scratch the skin to obtain relief. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychophysiology: The study of the physiological basis of human and animal behavior. [NIH]

Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]

Pulmonary: Relating to the lungs. [NIH] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of

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pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]

Pyramidal Tracts: Fibers that arise from cells within the cerebral cortex, pass through the medullary pyramid, and descend in the spinal cord. Many authorities say the pyramidal tracts include both the corticospinal and corticobulbar tracts. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Racemic: Optically inactive but resolvable in the way of all racemic compounds. [NIH] Radioactive: Giving off radiation. [NIH] Raphe Nuclei: Collections of small neurons centrally scattered among many fibers from the level of the trochlear nucleus in the midbrain to the hypoglossal area in the medulla oblongata. [NIH] Reaction Time: The time from the onset of a stimulus until the organism responds. [NIH] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]

Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rotenone: A botanical insecticide that is an inhibitor of mitochondrial electron transport. [NIH]

Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical

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structure, often a vessel or a nerve. [NIH] Scrapie: A fatal disease of the nervous system in sheep and goats, characterized by pruritus, debility, and locomotor incoordination. It is caused by proteinaceous infectious particles called prions. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Senile Plaques: Spherical masses consisting of amyloid fibrils and neuronal processes. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]

Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be

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expected to happen by chance alone. [NIH] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subiculum: A region of the hippocampus that projects to other areas of the brain. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substantia Innominata: Tissue in the base of the forebrain inferior to the anterior perforated substance, and anterior to the globus pallidus and ansa lenticularis. It contains the basal nucleus of Meynert. [NIH] Substrate: A substance upon which an enzyme acts. [EU] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatic treatment: Therapy that eases symptoms without addressing the cause of disease. [NIH] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptophysin: A 38-kDa integral membrane glycoprotein of the presynaptic vesicles in

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neuron and neuroendocrine cells. It is expressed by a variety of normal and neoplastic neuroendocrine cells and is therefore used as an immunocytochemical marker for neuroendocrine differentiation in various tumors. In Alzheimer disease and other dementing disorders there is an important synapse loss due in part to a decrease of synaptophysin in the presynaptic vesicles. [NIH] Systemic: Affecting the entire body. [NIH] Tau Proteins: One of the two major classes of microtubule-associated proteins isolated from the brain. The proteins have two domains: one that binds to microtubules and a second that binds to other cell components. By binding to several unpolymerized tubulin molecules simultaneously, tau proteins speed up the nucleation process in tubulin polymerization. Chemically modified tau proteins also appear to be involved in the formation and/or composition of the neurofibrillary tangles and neuropil threads found in Alzheimer disease. [NIH]

Telencephalon: Paired anteriolateral evaginations of the prosencephalon plus the lamina terminalis. The cerebral hemispheres are derived from it. Many authors consider cerebrum a synonymous term to telencephalon, though a minority include diencephalon as part of the cerebrum (Anthoney, 1994). [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Temporal Lobe: Lower lateral part of the cerebral hemisphere. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [NIH]

Thermal: Pertaining to or characterized by heat. [EU] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]

Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonic: 1. Producing and restoring the normal tone. 2. Characterized by continuous tension. 3. A term formerly used for a class of medicinal preparations believed to have the power of restoring normal tone to tissue. [EU]

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Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]

Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Tremor: Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of cerebellar diseases, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of Parkinson disease. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasodilator: An agent that widens blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the

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body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Wakefulness: A state in which there is an enhanced potential for sensitivity and an efficient responsiveness to external stimuli. [NIH] War: Hostile conflict between organized groups of people. [NIH] Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]

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INDEX 1 1-Methyl-4-phenyl-1,2,3,6tetrahydropyridine, 9, 65 A Acetylcholine, 17, 65, 69, 82 Acidity, 65, 84 Actin, 65, 81 Adaptability, 65, 69 Adrenal Glands, 65, 66 Adrenergic, 65, 73, 74, 88 Aerobic, 65, 80 Age of Onset, 55, 65, 68 Agonist, 65, 73 Amino acid, 65, 66, 72, 75, 76, 83, 84, 85, 87, 88, 90 Amino Acid Sequence, 65, 66 Amyloid, 7, 8, 10, 15, 17, 18, 24, 38, 39, 65, 69, 87 Amyloidosis, 38, 65 Anatomical, 12, 66, 69, 77, 86 Anemia, 66, 81 Angiopathy, 17, 66, 69 Animal model, 7, 66 Anions, 66, 78, 87, 88 Ansa, 66, 88 Antibacterial, 66, 87 Antibiotic, 66, 87 Antibodies, 33, 66, 77, 84 Antibody, 66, 70, 77, 79 Anticoagulant, 66, 85 Antigen, 66, 70, 77, 78, 79 Antimetabolite, 66, 72 Antioxidant, 66, 83 Antiviral, 67, 72 Apoptosis, 29, 67, 68 Arterial, 9, 67, 76, 78 Arteries, 66, 67, 68, 71, 78, 80 Arteriovenous, 67, 69 Artery, 67, 71, 78, 85, 90 Ataxia, 67, 69, 76 Atrophy, 9, 15, 16, 23, 34, 35, 67, 81 Autonomic, 19, 65, 67, 82, 83 Autopsy, 3, 8, 25, 67 Axons, 67, 72, 82 B Bacteria, 66, 67, 80, 87, 90 Bacteriophage, 67, 90 Basal Ganglia, 67, 68, 69, 77

Basement Membrane, 67, 74, 78 Benign, 54, 67, 68, 75 Benign tumor, 54, 67 Beta-pleated, 39, 65, 67 Biochemical, 5, 7, 24, 36, 66, 68, 87 Biological Transport, 68, 72 Bipolar Disorder, 12, 68 Bladder, 68, 77, 90 Blood Platelets, 68, 87 Blood vessel, 66, 68, 69, 78, 83, 89, 90 Bone Marrow, 68, 79, 81 Brain Neoplasms, 68, 76 Brain Stem, 68, 69, 81 C Carbon Dioxide, 68, 76 Carcinoma, 39, 68 Cardiac, 39, 68, 74, 81 Cardiovascular, 68, 87 Carpal Tunnel Syndrome, 39, 68 Case report, 4, 23, 24, 26, 68 Caspase, 7, 68 Catecholamine, 68, 73 Caudal, 68, 72, 77, 84 Cell, 5, 7, 9, 12, 32, 39, 65, 67, 68, 69, 70, 71, 72, 73, 74, 75, 78, 79, 80, 81, 82, 84, 86, 88, 89, 90 Cell Adhesion, 68, 78 Cell Death, 5, 9, 32, 67, 69, 81 Cell Respiration, 69, 80 Central Nervous System, 65, 68, 69, 75, 76, 78, 82, 84, 87 Central Nervous System Infections, 69, 75, 76 Cerebellar, 67, 69, 90 Cerebellar Diseases, 67, 69, 90 Cerebellum, 68, 69, 74, 84 Cerebral, 28, 35, 39, 67, 68, 69, 74, 76, 81, 83, 86, 89 Cerebral Cortex, 28, 67, 69, 81, 86 Cerebral Hemorrhage, 39, 69 Cerebrospinal, 6, 69, 76 Cerebrospinal fluid, 6, 69, 76 Cerebrovascular, 9, 69 Cerebrum, 69, 89 Character, 69, 71 Chin, 69, 80 Cholinergic, 42, 69 Chromatin, 67, 69

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Lewy Body Disease

Chronic, 39, 69, 77, 88 Circadian, 11, 69 Clinical Medicine, 70, 85 Clinical trial, 6, 13, 49, 70, 85 Coenzyme, 34, 70 Cognition, 5, 6, 32, 70 Collagen, 11, 65, 67, 70, 74, 85 Complement, 70, 78 Computational Biology, 49, 70 Computed tomography, 14, 35, 70, 71 Computerized axial tomography, 70, 71 Computerized tomography, 70, 71 Concomitant, 5, 14, 38, 71 Conjugated, 71 Connective Tissue, 68, 70, 71, 74, 75 Consciousness, 71, 72 Contraindications, ii, 71 Coronary, 71, 80 Coronary Thrombosis, 71, 80 Cortex, 6, 71, 73 Cortical, 5, 9, 15, 20, 21, 26, 32, 35, 43, 71 Craniocerebral Trauma, 69, 71, 75, 76 Criterion, 4, 71 Cytochrome, 27, 34, 71 Cytoplasm, 67, 71, 81 Cytoskeleton, 12, 71, 78, 80 D Degenerative, 4, 9, 21, 22, 34, 54, 71 Deletion, 67, 72 Delusions, 3, 5, 72 Dendrites, 72, 81, 82 Dentate Gyrus, 72, 76 Deoxyglucose, 26, 72 Diagnostic procedure, 37, 72 Dialyzer, 72, 75 Diencephalon, 72, 77, 81, 89 Diffusion, 12, 68, 72 Dilation, 72, 76 Direct, iii, 70, 72, 73, 79, 86, 88 Dissociation, 11, 72 Dissociative Disorders, 72 Distal, 72, 82 Dopa, 18, 72, 78 Dopamine, 9, 73, 78, 82 Dorsal, 11, 73, 84 Dorsum, 73 Dyes, 65, 73 Dystrophic, 32, 73 Dystrophy, 31, 73 E Effector, 65, 70, 73 Elastin, 70, 73

Electrons, 67, 73, 78, 83 Electrophoresis, 73, 84 Endocrine Glands, 73 Endogenous, 73 Endorphins, 73, 82 Enkephalins, 73, 82 Entorhinal Cortex, 73, 76 Environmental Health, 48, 50, 73 Enzyme, 68, 70, 73, 74, 88, 89, 91 Eosinophilic, 39, 74 Epidemiological, 38, 74 Epinephrine, 65, 73, 74, 82, 90 Epithelial, 68, 74, 78 Epithelial Cells, 74, 78 Estrogen, 7, 74 Eukaryotic Cells, 74, 90 Excitation, 74, 82 Extracellular, 39, 65, 71, 74, 77 Extracellular Matrix, 71, 74, 77 Extrapyramidal, 8, 21, 25, 73, 74 F Family Planning, 49, 74 Fat, 66, 68, 74, 79 Feasibility Studies, 7, 74 Fibril, 38, 74 Fibroblasts, 6, 74 Fibrosis, 74, 86 Fold, 13, 74 Fourth Ventricle, 74, 79 Free Radicals, 66, 72, 74 G Gait, 5, 69, 74 Ganglia, 65, 75, 81, 84 Gas, 68, 72, 75, 76, 82, 85 Gastrointestinal, 74, 75, 87, 88 Gastrointestinal tract, 75, 87 Gene, 10, 11, 18, 32, 75, 90 Genotype, 18, 75 Gland, 75, 83, 88, 89 Globus Pallidus, 75, 88 Glucose, 13, 72, 75, 77 Glutamate, 13, 75 Glutamic Acid, 75, 82, 85 Glycine, 65, 75, 82 Glycoprotein, 75, 78, 88, 89 Goats, 75, 87 Governing Board, 75, 84 Granule, 31, 72, 75 Growth factors, 75, 81 H Headache, 75, 76 Hematoxylin, 39, 75

95

Heme, 71, 75 Hemodialysis, 39, 72, 75 Hemostasis, 76, 78, 87 Hereditary, 39, 76, 81 Heredity, 75, 76 Heterodimers, 76, 77 Hippocampus, 7, 8, 22, 72, 76, 81, 88 Histology, 76, 81 Hormonal, 54, 67, 76 Hormone, 74, 76, 77, 89 Hydrocephalus, 54, 55, 76, 78 Hydrogen, 65, 76, 79, 80, 83, 84, 88 Hydrogen Peroxide, 76, 79, 88 Hydroxylysine, 70, 76 Hydroxyproline, 65, 70, 76 Hypertension, 69, 76, 78 Hyperventilation, 42, 76 Hypokinesia, 76, 83 Hypothalamus, 11, 68, 72, 77 I Idiopathic, 27, 34, 35, 77 Illusions, 5, 77 Immunohistochemistry, 28, 77 Impairment, 5, 8, 42, 67, 77, 82 In situ, 8, 77 In vitro, 7, 9, 28, 77, 89 In vivo, 9, 77 Incidental, 14, 16, 28, 29, 32, 36, 77 Incontinence, 35, 76, 77 Infarction, 69, 71, 76, 77, 78, 80 Infection, 54, 77, 79, 88 Inflammation, 39, 74, 77, 84 Innervation, 11, 77, 79 Inotropic, 73, 77 Insight, 12, 77 Insulin, 77, 78 Integrins, 12, 77 Intermediate Filaments, 78, 81 Intracellular, 7, 77, 78, 86 Intracranial Aneurysm, 69, 78 Intracranial Arteriosclerosis, 69, 78 Intracranial Hemorrhages, 76, 78 Intracranial Hypertension, 75, 76, 78 Ions, 65, 72, 76, 78 Ischemia, 67, 78 Islet, 39, 78 K Kb, 48, 78 L Laminin, 12, 67, 78 Latency, 11, 78 Lethargy, 19, 76, 78

Levo, 73, 78 Levodopa, 29, 73, 78 Ligands, 77, 79 Limbic, 29, 79 Lipid, 77, 79, 83 Lipid Peroxidation, 79, 83 Liver, 66, 79, 84 Lobe, 54, 79 Localization, 77, 79 Localized, 65, 77, 78, 79, 84 Locomotion, 79, 84 Locomotor, 11, 79, 87 Locus Coeruleus, 11, 79 Lucida, 78, 79 Lymphatic, 77, 79, 87 Lymphoid, 66, 79 M Malignancy, 39, 79 Malignant, 68, 79, 81 Malignant tumor, 79, 81 Malnutrition, 67, 79 Manic, 68, 79 Median Nerve, 68, 79 Mediate, 73, 79 Mediator, 73, 79, 87 Medical Records, 80, 86 MEDLINE, 49, 80 Medullary, 39, 80, 86 Megalencephaly, 18, 80 Melanin, 79, 80, 90 Membrane, 70, 72, 74, 78, 80, 88 Memory, 6, 42, 55, 72, 80 Mental, iv, 5, 6, 31, 48, 50, 54, 69, 70, 72, 77, 80, 85, 86 Mental Health, iv, 6, 48, 50, 80, 85 Mental Processes, 72, 80, 85 Mesencephalic, 79, 80 Metabolite, 9, 80 MI, 63, 80 Microorganism, 80, 91 Microtubule-Associated Proteins, 80, 81, 89 Microtubules, 78, 80, 81, 89 Mitochondria, 9, 80 Mitosis, 67, 80 Molecular, 9, 10, 12, 26, 29, 49, 51, 70, 72, 80, 81, 84, 86, 88 Molecule, 10, 66, 70, 72, 73, 74, 80, 83, 86, 90 Monitor, 80, 82 Morphological, 5, 31, 39, 80, 82 Motility, 80, 87

96

Lewy Body Disease

Motor nerve, 81, 82 Multiple Myeloma, 39, 81 Muscular Dystrophies, 73, 81 Myocardium, 80, 81 N Necrosis, 67, 77, 80, 81 Neocortex, 81 Neoplastic, 81, 89 Nerve, 10, 38, 54, 65, 67, 69, 72, 77, 79, 81, 82, 87, 88, 90 Nervous System, 69, 79, 81, 82, 83, 87, 88 Neural, 17, 21, 31, 34, 36, 65, 81 Neurites, 15, 27, 28, 32, 81 Neurodegenerative Diseases, 10, 12, 38, 81 Neuroendocrine, 81, 89 Neurofibrillary Tangles, 5, 9, 27, 31, 81, 82, 89 Neurofilaments, 81 Neurologic, 5, 76, 81 Neuromuscular, 65, 81, 82 Neuromuscular Junction, 65, 82 Neuronal, 6, 7, 10, 16, 28, 81, 82, 87 Neuronal Plasticity, 7, 82 Neurons, 9, 11, 27, 72, 75, 78, 81, 82, 86, 88 Neuropil, 28, 82, 89 Neuropil Threads, 28, 82, 89 Neuropsychology, 25, 42, 82 Neurotoxic, 10, 65, 82 Neurotransmitter, 5, 65, 73, 75, 82, 88 Norepinephrine, 65, 73, 82 Nuclear, 19, 22, 26, 67, 73, 74, 81, 82, 89 Nuclei, 11, 73, 80, 82 Nucleic acid, 82, 85 Nucleus, 67, 69, 71, 74, 75, 78, 79, 82, 86, 88 O Oculomotor, 23, 80, 82 Olfaction, 9, 82 Oncogenic, 78, 83 Optic Chiasm, 77, 83 Oxidation, 12, 67, 71, 79, 83 Oxidative Stress, 9, 27, 29, 83 P Palsy, 23, 28, 31, 34, 83 Pancreas, 77, 78, 83 Parietal, 8, 83 Parietal Lobe, 8, 83 Parkinsonism, 4, 5, 7, 11, 18, 23, 26, 78, 83 Particle, 83, 90 Pathogenesis, 7, 42, 83 Pathologic, 5, 67, 71, 83, 86 Pathologic Processes, 67, 83 Pathophysiology, 5, 12, 83

Patient Education, 54, 58, 60, 63, 83 Peptide, 10, 16, 17, 65, 83, 84, 85 Perfusion, 12, 19, 35, 83 Peripheral Nervous System, 73, 81, 82, 83, 88 PH, 14, 19, 35, 84 Pharmacologic, 84, 90 Phenyl, 9, 84 Phosphorylated, 70, 82, 84 Physiologic, 65, 73, 77, 84, 86, 90 Plants, 68, 75, 82, 84, 90 Plasma, 6, 66, 76, 81, 84, 87 Plasma cells, 66, 81, 84 Pleated, 84 Pneumonia, 71, 84 Polymorphism, 14, 27, 32, 84 Polypeptide, 65, 70, 84, 91 Pons, 8, 68, 74, 84 Posterior, 5, 8, 67, 69, 73, 83, 84 Postural, 4, 84 Practicability, 74, 84 Practice Guidelines, 50, 84 Prealbumin, 39, 84 Preclinical, 12, 84 Precursor, 7, 15, 38, 73, 78, 82, 85, 90 Presynaptic, 82, 85, 88 Prion, 39, 42, 69, 85 Progression, 12, 66, 85 Progressive, 5, 11, 19, 22, 23, 26, 28, 31, 34, 43, 72, 81, 85 Proline, 70, 76, 85 Protein C, 14, 65, 67, 85 Proteins, 9, 10, 11, 14, 19, 38, 65, 66, 68, 69, 70, 76, 78, 80, 81, 83, 84, 85, 86, 87, 89, 90 Proteinuria, 81, 85 Protocol, 8, 85 Pruritus, 85, 87 Psychiatric, 3, 4, 33, 54, 85 Psychiatry, 15, 16, 17, 18, 19, 21, 22, 23, 24, 25, 29, 32, 85, 88 Psychic, 80, 85 Psychology, 72, 82, 85 Psychophysiology, 82, 85 Public Health, 38, 50, 85 Public Policy, 49, 85 Publishing, 13, 42, 85 Pulmonary, 74, 76, 85, 90 Pulmonary Ventilation, 76, 85 Pulse, 12, 80, 85 Pyramidal Tracts, 74, 86 R Race, 72, 86

97

Racemic, 72, 86 Radioactive, 76, 82, 83, 86 Raphe Nuclei, 11, 86 Reaction Time, 9, 86 Receptor, 7, 17, 66, 73, 86, 87 Receptors, Serotonin, 86, 87 Recombinant, 28, 86, 90 Rectum, 75, 77, 86 Recurrence, 68, 86 Refer, 1, 70, 73, 79, 81, 86 Refraction, 86, 87 Reliability, 4, 86 Remission, 68, 86 Resorption, 76, 86 Retrospective, 3, 86 Retrospective study, 3, 86 Risk factor, 8, 86 Rotenone, 9, 86 S Schizophrenia, 12, 86 Sclerosis, 12, 21, 23, 78, 86 Scrapie, 39, 87 Screening, 70, 87 Senile, 25, 26, 34, 39, 82, 87 Senile Plaques, 25, 82, 87 Serotonin, 11, 82, 86, 87, 90 Serum, 34, 70, 84, 87 Serum Albumin, 84, 87 Side effect, 87, 90 Skeletal, 81, 87 Skull, 71, 87, 89 Specialist, 56, 72, 87 Species, 7, 74, 80, 86, 87, 88, 91 Spectrum, 11, 31, 34, 35, 87 Spinal cord, 68, 69, 79, 81, 83, 86, 87 Spleen, 66, 79, 87 Sporadic, 81, 87 Staging, 8, 12, 87 Statistically significant, 4, 87 Stimulus, 74, 77, 78, 86, 88 Stool, 77, 88 Stress, 9, 12, 32, 43, 68, 83, 88 Stupor, 78, 88 Subacute, 77, 88 Subclinical, 77, 88 Subiculum, 76, 88 Subspecies, 87, 88 Substance P, 80, 88 Substantia Innominata, 8, 88 Substrate, 23, 88 Superoxide, 8, 88 Superoxide Dismutase, 8, 88

Sympathomimetic, 73, 74, 82, 88 Symptomatic, 41, 88 Symptomatic treatment, 41, 88 Synapse, 35, 65, 82, 85, 88, 89, 90 Synaptic, 82, 88 Synaptophysin, 8, 88 Systemic, 66, 74, 77, 78, 81, 89 T Tau Proteins, 82, 89 Telencephalon, 67, 69, 89 Temporal, 8, 35, 36, 54, 76, 89 Temporal Lobe, 36, 89 Thalamus, 11, 68, 72, 89 Thermal, 72, 89 Thrombin, 85, 89 Thrombomodulin, 85, 89 Thrombosis, 78, 89 Thyroid, 39, 89, 90 Tissue, 6, 8, 10, 11, 66, 67, 68, 71, 74, 79, 80, 81, 82, 83, 87, 88, 89, 91 Tissue Culture, 10, 81, 89 Tomography, 13, 19, 26, 27, 89 Tone, 5, 89 Tonic, 5, 89 Tonus, 89, 90 Toxic, iv, 38, 73, 90 Toxicology, 50, 90 Toxins, 66, 77, 90 Trachea, 89, 90 Transduction, 12, 90 Transgenes, 38, 90 Transmitter, 65, 73, 79, 82, 90 Trauma, 81, 90 Tremor, 5, 80, 83, 90 Tryptophan, 70, 87, 90 Tyrosine, 73, 90 U Ubiquitin, 8, 9, 18, 20, 25, 28, 33, 81, 90 Urinary, 76, 77, 90 Urine, 68, 77, 85, 90 V Vascular, 8, 12, 31, 54, 77, 78, 90 Vasodilator, 73, 90 Vector, 90 Vein, 67, 82, 90 Ventral, 77, 82, 84, 90 Ventricle, 76, 77, 86, 89, 90, 91 Ventricular, 76, 91 Veterinary Medicine, 49, 91 Villi, 76, 91 Viral, 83, 90, 91 Virus, 67, 69, 90, 91

98

Lewy Body Disease

Vitro, 7, 91 Vivo, 91 W Wakefulness, 11, 91 War, 12, 91 Windpipe, 89, 91

Wound Healing, 78, 91 X Xenograft, 66, 91 X-ray, 10, 39, 70, 71, 82, 91 Z Zymogen, 85, 91

99

100

Lewy Body Disease

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