<mml:math id="E1" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>β</mml:mi></mml:math>-Amyloid Degradation and Alzheimer's Disease

Wang, Deng-Shun; Dickson, Dennis W.; Malter, James S.

doi:https://doi.org/10.1155/JBB/2006/58406

BioMed Research International

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Neurodegenerative Diseases: Mechanisms and Therapies

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Review Article | Open Access

Volume 2006 | Article ID 058406 | https://doi.org/10.1155/JBB/2006/58406

β-Amyloid Degradation and Alzheimer's Disease

Deng-Shun Wang,¹Dennis W. Dickson,²and James S. Malter^1,3

Received18 Nov 2005

Revised18 Jan 2006

Accepted01 Feb 2006

Published06 Apr 2006

Abstract

Extensive β-amyloid (Aβ) deposits in brain parenchyma in the form of senile plaques and in blood vessels in the form of amyloid angiopathy are pathological hallmarks of Alzheimer's disease (AD). The mechanisms underlying Aβ deposition remain unclear. Major efforts have focused on Aβ production, but there is little to suggest that increased production of Aβ plays a role in Aβ deposition, except for rare familial forms of AD. Thus, other mechanisms must be involved in the accumulation of Aβ in AD. Recent data shows that impaired clearance may play an important role in Aβ accumulation in the pathogenesis of AD. This review focuses on our current knowledge of Aβ-degrading enzymes, including neprilysin (NEP), endothelin-converting enzyme (ECE), insulin-degrading enzyme (IDE), angiotensin-converting enzyme (ACE), and the plasmin/uPA/tPA system as they relate to amyloid deposition in AD.

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Copyright © 2006 Deng-Shun Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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