The amyloid cascade hypothesis, the most widely accepted theory for the molecular sequence of pathological events in AD, postulates that the initial tissue changes in the AD brain involve the aggregation and deposition of the Aβ peptide [33], while the hyperphosphorylation and polymerization of tau into NFTs, NThs, Nts and, ultimately, neuronal loss would occur later. This evidence concerns the gene MAPT and Alzheimer disease.