The pathogenesis of Alzheimer's disease (AD) is characterized by several hallmarks, including abnormal processing of the amyloid precursor protein (APP), resulting in the deposition of amyloid beta (Aβ),1, 2 and the hyperphosphorylation of the tau protein (p‐tau), leading to the formation of neurofibrillary tangles in the brain.3 The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.