β-Amyloid degradation and Alzheimer's disease

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

Research output: Contribution to journalReview article

131 Scopus citations

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 Aβaccumulation 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.

Original languageEnglish (US)
Article number58406
JournalJournal of Biomedicine and Biotechnology
Volume2006
DOIs
StatePublished - 2006

ASJC Scopus subject areas

  • Biotechnology
  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Health, Toxicology and Mutagenesis

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