AD is characterized by brain atrophy, amyloid plaques [formed by accumulation of extracellular amyloid-β (Aβ) peptides, which derived from the cleavage of amyloid precursor protein (APP) with the help of presenilin-1 (PS1)], intracellular neurofibrillary tangles (formed by the deposition of hyperphosphorylated tau), with loss of neurons and synapses, and dystrophic neuritis (Tang and Le, 2016; Sarlus and Heneka, 2017; Hansen et al., 2018). This evidence concerns the gene APP and Alzheimer disease.