Abstract

Genetic studies have provided important insights into the pathogenesis of Alzheimer´s disease (AD). In the early 1990s, the identification of mutations in the amyloid precursor protein (APP), presenilin1 (PSEN1) and presenilin2 (PSEN2) genes – genes that encode proteins that are involved in the amyloidogenic processing of APP – as causative of monogenic AD provided strong arguments for the amyloid cascade hypothesis. According to the amyloid cascade hypothesis, amyloid beta (Aβ) accumulation and deposition occurs in late onset AD due to [...]

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