Movement Disorders (revue)

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Amyloid β‐peptide and the dementia of Parkinson's diease

Identifieur interne : 005711 ( Main/Exploration ); précédent : 005710; suivant : 005712

Amyloid β‐peptide and the dementia of Parkinson's diease

Auteurs : Jendroska [Allemagne] ; Andrew Lees (neurologue) [Royaume-Uni] ; Werner Poewe [Autriche] ; Susan E. Daniel [Royaume-Uni]

Source :

RBID : ISTEX:E82192D3EE94337E797CB52CDC2F7EC025A6806D

English descriptors

Abstract

It is not known whether an increased incidence of dementia in patients with Parkinson's disease (PD) is due to a higher incidence of Alzheimer's disease (AD) or to “early” Alzheimer‐type pathology. To determine whether amyloid β‐peptide (Aβ) of AD occurs more frequently in brains of patients with PD, we examined 50 cases and 79 controls by using histoblots for Aβ. Twentythree cases with PD had dementia, including all nine with Aβ distributed throughout the entire cerebral cortex; three of these cases had AD. In contrast, five of 17 controls with comparable Aβ accumulation were not demented. Neither AD nor Aβ deposition was increased in PD; furthermore, there was no statistical correlation between the amount of Aβ and the number of Lewy bodies in cerebral cortex. In 14 patients with PD in whom dementia was unrelated to Aβ, there was cerebral vascular disease (four), numerous cortical Lewy bodies (three), or hydrocephalus (two); in five further cases, dementia was not well explained by histopathologic changes. Our data found no increase of either AD or “early” Alzheimer‐type pathology in cases of PD; however, a synergistic effect between the two pathologies was suggested as contributing to dementia.

Url:
DOI: 10.1002/mds.870110609


Affiliations:


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Le document en format XML

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<div type="abstract" xml:lang="en">It is not known whether an increased incidence of dementia in patients with Parkinson's disease (PD) is due to a higher incidence of Alzheimer's disease (AD) or to “early” Alzheimer‐type pathology. To determine whether amyloid β‐peptide (Aβ) of AD occurs more frequently in brains of patients with PD, we examined 50 cases and 79 controls by using histoblots for Aβ. Twentythree cases with PD had dementia, including all nine with Aβ distributed throughout the entire cerebral cortex; three of these cases had AD. In contrast, five of 17 controls with comparable Aβ accumulation were not demented. Neither AD nor Aβ deposition was increased in PD; furthermore, there was no statistical correlation between the amount of Aβ and the number of Lewy bodies in cerebral cortex. In 14 patients with PD in whom dementia was unrelated to Aβ, there was cerebral vascular disease (four), numerous cortical Lewy bodies (three), or hydrocephalus (two); in five further cases, dementia was not well explained by histopathologic changes. Our data found no increase of either AD or “early” Alzheimer‐type pathology in cases of PD; however, a synergistic effect between the two pathologies was suggested as contributing to dementia.</div>
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