These compounds can interfere with various aspects of AD pathogenesis, such as the amyloid cascade hypothesis attributing AD to beta‐amyloid (Aβ) plaques and tau protein tangles, the cholinergic hypothesis linking it to a decline in acetylcholine transmission, and the infection hypothesis suggests chronic infections triggering immune activation and inflammation [25, 26, 27]. The gene discussed is MAPT; the disease is Alzheimer disease.