According to the amyloid hypothesis, which dominated the research of AD pathogenesis for more than 20 years, accumulation of soluble amyloid β (Aβ) into toxic oligomers and amyloid plaques initiates a pathogenic cascade leading to accumulation of the hyperphosphorylated tau protein in neurofibrillary tangles, to mitochondrial dysfunction, loss of synapses, neuronal cell death, and, ultimately, a loss of cognitive function [1–3]. This evidence concerns the gene MAPT and Alzheimer disease.