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Alzheimer's Research & Therapy
Published in: Alzheimer's Research & Therapy 2/2012

01-04-2012 | Review

Examining the mechanisms that link β-amyloid and α-synuclein pathologies

Authors: Samuel E Marsh, Mathew Blurton-Jones

Published in: Alzheimer's Research & Therapy | Issue 2/2012

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Abstract

β-amyloid (Aβ) and α-synuclein (α-syn) are aggregation-prone proteins typically associated with two distinct neurodegenerative disorders: Alzheimer's disease (AD) and Parkinson's disease. Yet α-syn was first found in association with AD plaques several years before being linked to Parkinson's disease or Lewy body formation. Nowadays, a large subset of AD patients (~50%) is well recognized to co-exhibit significant α-syn Lewy body pathology. Unfortunately, these AD Lewy body variant patients suffer from additional symptoms and an accelerated disease course. Basic research has begun to show that Aβ and α-syn may act synergistically to promote the aggregation and accumulation of each other. While the exact mechanisms by which these proteins interact remain unclear, growing evidence suggests that Aβ may drive α-syn pathology by impairing protein clearance, activating inflammation, enhancing phosphorylation, or directly promoting aggregation. This review examines the interactions between Aβ and α-syn and proposes potential mechanistic links between Aβ accumulation and α-syn pathogenesis.
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Metadata
Title
Examining the mechanisms that link β-amyloid and α-synuclein pathologies
Authors
Samuel E Marsh
Mathew Blurton-Jones
Publication date
01-04-2012
Publisher
BioMed Central
Published in
Alzheimer's Research & Therapy / Issue 2/2012
Electronic ISSN: 1758-9193
DOI
https://doi.org/10.1186/alzrt109

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