The amyloid cascade hypothesis, which was first proposed in 1992, and which continues to be the leading model of AD pathogenesis, points to the deposition of amyloid-beta (Aβ) plaques in the brain as the initiating step of AD pathogenesis, which in turn leads to the accumulation of neurofibrillary tangles composed of hyperphosphorylated tau, synaptic and neuronal dysfunction and loss, and cognitive decline [15,16]. This evidence concerns the gene MAPT and Alzheimer disease.