Alzheimer’s disease (AD) is defined, in part, by the appearance of extracellular amyloid deposits. Supported by genetic studies, the amyloid cascade is a leading hypothesis for the cause and pathogenesis of AD. Despite the intensive efforts that have been made in understanding amyloid and other pathological processes in AD, current approved interventions for AD have shown only modest effects in modifying clinical symptoms; none have been efficacious for slowing disease progression as demonstrated through clinical outcome measures.

Recent developments in the field of genetics have significantly advanced understanding of the etiology of AD. More than two dozen genes are now known to be associated with late-onset AD (LOAD). Using a combination of genome-wide association studies (GWAS),

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