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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 SeparovicThe 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 chemistryVolume
57Issue
6Pagination
511 - 518Publisher
CSIRO PublishingLocation
Collingwood, Vic.Publisher DOI
ISSN
0004-9425eISSN
1445-0038Language
engPublication classification
C1.1 Refereed article in a scholarly journalCopyright notice
2004, CSIROUsage metrics
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