Although the pathogenesis of AD is still not fully elucidated, studies have revealed that the AD brain exhibits β-amyloid peptide (Aβ) plaques, neurofibrillary tangles formed by the accumulation of hyperphosphorylated microtubule-associated protein tau, glial cell activation, neuroinflammation, and the loss of neurons and synapses [53]. The gene discussed is MAPT; the disease is Alzheimer disease.