Aβ accumulation in the brain has been proposed as a potential trigger for AD and has formed the traditional ‘amyloid hypothesis’, which suggests that a defect in Aβ metabolism in the aged brain leads to a linear sequence of events involving the accumulation of toxic Aβ and the formation of amyloid fibrils that subsequently develop into senile plaques and trigger tau pathology and neurotoxicity [193]. This evidence concerns the gene MAPT and Alzheimer disease.