File(s) not publicly available

Metal-catalyzed oxidative damage and oligomerization of the amyloid-β peptide of Alzheimer’s disease

journal contribution
posted on 2004-01-01, 00:00 authored by F Ali, K Barnham, Colin BarrowColin Barrow, F Separovic
The most common form of dementia in old age is Alzheimer’s disease (AD). The presence in the brain of senile plaque is the major pathological marker of AD. The plaques are primarily composed of aggregated amyloid-β peptide (Aβ). Aβ is a 40–42 amino acid peptide that is a proteolytic product derived from the β-amyloid precursor protein. The function of Aβ and the exact mechanism of Aβ aggregation and neurotoxicity are unclear. However, metal coordination by Aβ plays an important role in inducing aggregation and the generation of reactive oxygen species, which appears to be at least partially responsible for Aβ neurotoxicity. In this review we examine the role of copper and zinc ions in Aβ neurotoxicity, especially with regards to the generation of free radicals. We discuss the role of copper or zinc ions in oxidative damage and Aβ conformational changes and the relationship of these metals to AD.

History

Journal

Australian journal of chemistry

Volume

57

Issue

6

Pagination

511 - 518

Publisher

CSIRO Publishing

Location

Collingwood, Vic.

ISSN

0004-9425

eISSN

1445-0038

Language

eng

Publication classification

C1.1 Refereed article in a scholarly journal

Copyright notice

2004, CSIRO

Usage metrics

Categories

Keywords

Exports