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Vol. 17, Suppl. 1, 2004
Issue release date: December 2003
Section title: Paper
Dement Geriatr Cogn Disord 2004;17(suppl 1):3–14
(DOI:10.1159/000074677)

Pathology and Neurotransmitter Abnormalities of Dementia with Lewy Bodies

Duda J.E.
Parkinson’s Disease Research, Education and Clinical Center, Philadelphia VA Medical Center, and the Department of Neurology, University of Pennsylvania, Philadelphia, Pa., USA

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 12/19/2003
Issue release date: December 2003

Number of Print Pages: 12
Number of Figures: 4
Number of Tables: 2

ISSN: 1420-8008 (Print)
eISSN: 1421-9824 (Online)

For additional information: http://www.karger.com/DEM

Abstract

The neuropathology of dementia with Lewy bodies (DLB) is characterized by the presence of Lewy bodies (LBs) and Lewy neurites (LNs) in specific systems throughout the brainstem, diencephalon, basal ganglia and neocortex. DLB shares many features with Parkinson’s disease (PD) with respect to LB distribution in the brainstem, and there is recent evidence that Lewy pathology (LP), which consists of LBs and LNs, may progress in a systematic fashion through the brain regardless of clinical phenotype. Increasing evidence supports a central role for LNs in Lewy neurodegeneration and engenders a ‘neuritic dystrophy hypothesis’ described herein. LP formation also occurs in Alzheimer’s disease (AD) and other dementias, and it is unclear whether there is a common underlying pathophysiology in these diseases or if the LP merely represents a common final pathway. Cholinergic deficits are evident in both DLB and AD, with reductions in acetylcholine and abnormalities in nicotinic and muscarinic receptor expression in both diseases. Cholinergic deficits are greater in DLB than in AD, although generally there is less brain atrophy in DLB. The lower neurodegeneration and preservation of cholinergic receptors in DLB has important therapeutic implications because patients with DLB (vs. AD) may receive greater benefits from cholinergic pharmacologic therapy. Patients with DLB who display parkinsonian signs have severe dopamine neurotransmitter deficiencies similar to those in patients with PD, although the manifestation of these deficiencies is different. Both groups have striatal dopamine transporter deficiencies, but the striatal dopamine D2 receptors are reduced in DLB patients compared with PD and control subjects. D2 receptor deficiencies in DLB may be the cause of the relative lack of response to levodopa treatment and the severe adverse reaction to neuroleptics in these patients.

© 2004 S. Karger AG, Basel


  

Author Contacts

John E. Duda, MD, Co-Director
Parkinson’s Disease Research, Education and Clinical Center
Philadelphia VA Medical Center, 3900 Woodland Avenue
Philadelphia, PA 19104 (USA)
Tel. +1 215 823 5934, Fax +1 215 823 5815, E-Mail John.Duda@med.va.gov

  

Article Information

Number of Print Pages : 12
Number of Figures : 4, Number of Tables : 2, Number of References : 102

  

Publication Details

Dementia and Geriatric Cognitive Disorders

Vol. 17, No. Suppl. 1, Year 2004 (Cover Date: Released December 2003)

Journal Editor: V. Chan-Palay, New York, N.Y.
ISSN: 1420–8008 (print), 1421–9824 (Online)

For additional information: http://www.karger.com/journals/dem


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 12/19/2003
Issue release date: December 2003

Number of Print Pages: 12
Number of Figures: 4
Number of Tables: 2

ISSN: 1420-8008 (Print)
eISSN: 1421-9824 (Online)

For additional information: http://www.karger.com/DEM


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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