Pathophysiology of AD includes the oxidative state, the aggregation of pathological amyloid-β (Aβ), and abnormal accumulation of hyperphosphorylated neurofibrillary tangles of the tau protein, followed by inflammation in the central cortex and limbic system of the brain, which results in neuronal atrophy and a loss of synapses [5,6]. This evidence concerns the gene MAPT and Alzheimer disease.