The physiopathology of AD is characterized by two pathological hallmarks: within neurons, the accumulation of hyperphosphorylated Tau protein leads to the formation of neurofibrillary tangles [1]; in the extraneuronal environment, the abnormal proteolytic processing of the amyloid precursor protein (APP) leads to the aggregation of senile plaques, or amyloid plaques. The gene discussed is APP; the disease is Alzheimer disease.