Alzheimer’s disease is categorized by neuroinflammation, mitochondrial impairment, synaptic dysfunction, oxidative stress, and disruption in the blood–brain barrier, which may be due to uncharacteristic extracellular buildup and deposition of the amyloid-β peptide (Aβ) in amyloid plaques and accumulation of neuronal hyperphosphorylated tau protein in intracellular neurofibrillary tangles (NFTs) [16]. This evidence concerns the gene MAPT and Alzheimer disease.