Journal
BIOMOLECULES
Volume 4, Issue 1, Pages 101-116Publisher
MDPI
DOI: 10.3390/biom4010101
Keywords
amyloid-metal effects; amyloid aggregation; multiple pathways kinetics; Alzheimer's disease
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Funding
- Natural Sciences and Engineering Research Council of Canada (NSERC)
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Metal ions, including copper and zinc, have been implicated in the pathogenesis of Alzheimer's disease through a variety of mechanisms including increased amyloid-beta affinity and redox effects. Recent reports have demonstrated that the amyloid-beta monomer does not necessarily travel through a definitive intermediary en-route to a stable amyloid fibril structure. Rather, amyloid-beta misfolding may follow a variety of pathways resulting in a fibrillar end-product or a variety of oligomeric end-products with a diversity of structures and sizes. The presence of metal ions has been demonstrated to alter the kinetic pathway of the amyloid-beta peptide which may lead to more toxic oligomeric end-products. In this work, we review the contemporary literature supporting the hypothesis that metal ions alter the reaction pathway of amyloid-beta misfolding leading to more neurotoxic species.
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