Abstract
The Alzheimer‘s disease amyloid precursor protein is sequentially processed to yield the neurotoxic amyloid-β (Aβ) peptide, which is the principal component of the senile plaques in Alzheimer‘s disease brains. This review will outline the current thinking on how Aβ mediates neurotoxicity or neuronal dysfunction. In particular, this article will focus on the key residues that modulate Aβ‘s activity and the cellular pathways and mechanisms involved. It will detail how Aβ–metal interactions are a key determinate in Alzheimer‘s disease pathogenesis.