Several hypotheses have been developed to explain the pathogenesis and progression of AD, such as amyloid-β (Aβ) deposits [2], tau protein aggregation [3], neuroinflammation [4], mitochondrial dysfunction [5], cholinergic dysfunction [6], etc. The cholinergic hypothesis suggests that in AD pathological conditions, cholinergic neurons are extensively damaged and die, and the activity of choline acetyltransferase is significantly reduced. The gene discussed is MAPT; the disease is Alzheimer disease.