At the pathological level, AD is characterized by the deposition of extracellular amyloid-beta (Aβ) and the formation of intracellular tangles of neuronal fibers composed of hyperphosphorylated tau proteins that are highly coiled within neurons.[17,18] The plaques formed by Aβ deposits and hyperphosphorylated tau protein disrupt the normal function of neurons and synapses, representing the classic pathogenesis of AD.[19,20] Moreover, the pathogenesis of AD also involves complex processes such as oxidative stress, neuroinflammation, dysautophagy, and neuronal apoptosis (Fig. 1). This evidence concerns the gene MAPT and Alzheimer disease.