Journal of Biomedicine and Biotechnology
Volume 2006 (2006), Article ID 58406, 12 pages
doi:10.1155/JBB/2006/58406
Review Article

β-Amyloid Degradation and Alzheimer's Disease

Deng-Shun Wang,1 Dennis W. Dickson,2 and James S. Malter1,3

1Department of Pathology and Laboratory Medicine, School of Medicine, University of Wisconsin, Madison 53705, WI, USA
2Departments of Pathology (Neuropathology) and Neuroscience, Mayo Clinic College of Medicine, Jacksonville 32224, FL, USA
3Waisman Center for Developmental Disabilities, School of Medicine, University of Wisconsin, Madison 53705, WI, USA

Received 18 November 2005; Revised 18 January 2006; Accepted 1 February 2006

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.

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.