Cover

Dementia in Clinical Practice

Editor(s): Giannakopoulos P. (Geneva) 
Hof P.R. (New York, N.Y.) 
Table of Contents
Vol. 24, No. , 2009
Section title: Lewy Body Dementia
Giannakopoulos P, Hof PR (eds): Dementia in Clinical Practice. Front Neurol Neurosci. Basel, Karger, 2009, vol 24, pp 114–125
(DOI:10.1159/000197890)

Significance of Brain Lesions in Parkinson Disease Dementia and Lewy Body Dementia

Jellinger K.A.
Institute of Clinical Neurobiology, Vienna, Austria

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Article / Publication Details

First-Page Preview
Abstract of Lewy Body Dementia

Published online: 1/26/2009
Cover Date: 2009

Number of Print Pages: 12
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-9015-0 (Print)
eISBN: 978-3-8055-9016-7 (Online)

Abstract

Dementia is increasingly recognized as a common feature in patients with Parkinson disease (PD)and dementia with Lewy bodies (DLB), both sharing many clinical and morphological features andbelieved to form a continuum within the spectrum of Lewy body diseases. Based on a large autopsyseries of parkinsonism (31–37% with dementia) and review of the recent literature, the pathologicalchanges underlying cognitive impairment in PD with dementia (PDD) and DLB are discussed. PDcases with Lewy body stages 3–5, i.e. only mild to moderate cortical -synuclein (Syn) depositions,and no additional pathologies, are rarely associated with cognitive impairment, which is frequentlyseen in PD and DLB cases with considerable cortical and limbic Syn load (increasing Lewy bodydensities) and/or associated widespread Alzheimer-type pathology. Clinicopathological studiesshow a negative relation between cognitive impairment and both cortical Lewy body pathology andAlzheimer type changes, suggesting that these either alone or in combination are major causes ofcognitive dysfunction, while others related them to presynaptic Syn aggregates. The neuropathologyof PDD and DLB is similar, without significant differences between cortical and subcortical Lewybodies and the pattern of synuclein pathology in the brainstem, but there are topographic differencesin nigral lesions, more frequent affection of the hippocampal CA 2/3 subareas and more severediffuse amyloid plaque load in the striatum of DLB. In conclusion, the pathology underlying cognitiveimpairment in PDD and DLB is heterogeneous, but there are some differences in the topographyand severity of lesions between both phenotypes that need further evaluation.


  

Author Contacts

Kurt A. Jellinger, MD
Institute of Clinical Neurobiology
Kenyongasse 18
AT–1070 Vienna (Austria)
Tel./Fax +43 1 526 6534
E-Mail kurt.jellinger@univie.ac.at

  

Article Information

Number of Print Pages : 12

  

Publication Details

Book Serie: Frontiers of Neurology and Neuroscience, Vol. 24, Year 2009

Editor(s): Bogousslavsky, J. (Montreux)
ISSN: 1660-4431 (Print), eISSN: 1662-2804 (Online)

For additional information:
http://content.karger.com/ProdukteDB/produkte.asp?issn=1660-4431

Book Title: Dementia in Clinical Practice

Editor(s): Giannakopoulos P, Hof PR (eds)

For additional information:
http://content.karger.com/ProdukteDB/produkte.asp?issn=1660-4431&volume=24


Article / Publication Details

First-Page Preview
Abstract of Lewy Body Dementia

Published online: 1/26/2009
Cover Date: 2009

Number of Print Pages: 12
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-9015-0 (Print)
eISBN: 978-3-8055-9016-7 (Online)


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