These genetic alterations accelerate the pathological characteristics of AD, including the formation of extracellular amyloid plaques and the formation of intracellular neurofibrillary tangles consisting of hyperphosphorylated tau. The accumulation of these amyloid plaques are not only a crucial factor in the pathology of AD [1], but have been argued to contribute to the distinctive clinical symptoms of AD such as progressive cognitive decline, loss of memory and decreased mental capacity [2,3]. The gene discussed is MAPT; the disease is Alzheimer disease.