
TY  - JOUR
A1  - Ali, Feda E. A. 
A1  - Barnham, Kevin J. 
A1  - Barrow, Colin J. 
A1  - Separovic, Frances 
T1  - Metal-Catalyzed Oxidative Damage and Oligomerization of the Amyloid-&#946; Peptide of Alzheimer&#8217;s Disease
JF  - Australian Journal of Chemistry
JO  - Aust. J. Chem.
Y1  - 2004
VL  - 57
IS  - 6
SP  - 511
EP  - 518
KW  - 
UR  - https://doi.org/10.1071/CH04026 
N2  - The most common form of dementia in old age is Alzheimer&#8217;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-&#946; peptide (A&#946;). A&#946; is a 40&#8211;42 amino acid peptide that is a proteolytic product derived from the &#946;-amyloid precursor protein. The function of A&#946; and the exact mechanism of A&#946; aggregation and neurotoxicity are unclear. However, metal coordination by A&#946; plays an important role in inducing aggregation and the generation of reactive oxygen species, which appears to be at least partially responsible for A&#946; neurotoxicity. In this review we examine the role of copper and zinc ions in A&#946; neurotoxicity, especially with regards to the generation of free radicals. We discuss the role of copper or zinc ions in oxidative damage and A&#946; conformational changes and the relationship of these metals to AD. 
ER  -

