AD is characterized by cognitive deficits, impairment of activities of daily living, and behavioral disturbances [1], and has two major pathological hallmarks, the presence of extracellular senile plaques caused by accumulation of Aβ, and the intracellular neurofibrillary tangles formed from the deposition of hyper-phosphorylated tau protein [2–4]. This evidence concerns the gene MAPT and Alzheimer disease.