Although current hypotheses emphasize different mechanisms, such as Aβ deposition, tau hyperphosphorylation, oxidative stress, neuroinflammation, and altered cholinergic and glutamatergic neurotransmission, the Aβ cascade and tau aggregation remain the most widely accepted central factors that trigger and/or accelerate AD pathogenesis. The gene discussed is MAPT; the disease is Alzheimer disease.