The extracellular deposition of accumulated amyloid beta (Aβ) peptide (i.e., the 42 amino acid-long Aβ peptide [Aβ1–42]) in the form of diffuse and neuritic Aβ plaques and the intraneuronal accumulation of neurofibrillary tangles (NFTs), consisting of aggregated hyperphosphorylated tau (p-tau) proteins, are the key pathophysiological hallmarks detected in AD brains [11]. This evidence concerns the gene MAPT and Alzheimer disease.