The two most popular theories for the pathogenesis of AD are the excess and aggregation of Aβ peptide in the form of plaques and microtubule-associated tau protein becoming abnormally hyperphosphorylated and forms NFT that accumulates in the brain of AD; however, synaptic disturbance for calcium influx, autophagy, microgliosis–astrogliosis, and neuron demyelination are considered major factors in AD pathophysiology (Figure 1). This evidence concerns the gene MAPT and Alzheimer disease.