Abstract
The onset and progression of Alzheimer's disease is characterized by the aggregation of the 42-residue form of the amyloid-β peptide (Aβ42). Significant evidence indicates that the mechanism by which Aβ42 induces cell death is through the interaction of its toxic oligomeric species with cell membranes, which results in the disruption of membrane integrity and homeostatic processes within the cell. Moreover, there is evidence that Aβ42 interacts differentially with regions of membranes enriched in different cell membrane components, and that its cytotoxicity is increased as the size of the oligomers decreases and their hydrophobicity increases.
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