The amyloid cascade hypothesis posits that in the context of AD, amyloid precursor protein (APP) is predominantly hydrolyzed by β-site APP cleavage enzyme 1 (BACE1) and γ-secretase, leading to the production of soluble Aβ monomers, which subsequently form toxic oligomers or fibrils. The gene discussed is BACE1; the disease is Alzheimer disease.