The core pathophysiology of AD has been postulated as the intraneuronal aggregation of hyperphosphorylated tau, a microtubule-associated protein, which leads to the formation of neurofibrillary tangles, and the interstitial aggregation of insoluble forms of the amyloid-β (Aβ) peptide, which results in neuritic plaques [1]. This evidence concerns the gene MAPT and Alzheimer disease.