The disease is characterized by distinct neuropathological hallmarks, including extracellular accumulation of β-amyloid peptide-containing plaques (senile plaques) in cerebral cortical regions of AD patients [3], intracellular aggregation of hyperphosphorylated Tau proteins resulting in neurofibrillary tangles [4], and significant synaptic loss [5], and neuronal degeneration [6]. This evidence concerns the gene MAPT and Alzheimer disease.