The main pathological feature of AD is the presence of a large number of senile plaques with extracellular Aβ as the main component in the cerebral cortex and hippocampus senile plaque (SP) and neurofibrillary tangles (NFTs) with hyperphosphorylated Tau (P-Tau) as the main component, leading to severe impairment of neuronal function and synaptic capacity in specific brain regions, cognitive decline and memory impairment [2]. This evidence concerns the gene MAPT and Alzheimer disease.