Abstract
Amyloidogenic diseases are characterized by the toxic misfolding and self-assembly of intrinsically disordered proteins into insoluble aggregates known as amyloids. Amyloid fibrils and oligomers are implicated in a wide variety of human diseases, including type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD). Mitochondrial dysfunction is a hallmark of amyloid toxicity and is attributed to the aggregation of amyloidogenic proteins, including human islet amyloid polypeptide (hIAPP) in T2DM and amyloid-β (Aβ) in AD.
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