Abstract
Epidemiological studies establish a link between Type 2 diabetes (T2DM) and Alzheimer's disease (AD), both leading causes of morbidity and mortality in the elderly. These diseases also share clinical and biochemical features suggesting common pathogenic mechanisms. Specifically, both are amyloidoses as they are characterized by fibrillar protein aggregates - amylin in T2DM pancreatic islets, and beta-amyloid (Abeta) and neurofibrillary tangles (NFTs) in AD brain. Amylin aggregation is associated with pancreatic beta-cell loss, and Abeta and NFT formation with neuronal cell loss. We discuss the possibility that amylin and Abeta exert their toxicity by similar mechanisms, with components of the pathocascades shared, and that therapies based on amyloidogenic properties are beneficial for both T2DM and AD.