While the cause of AD continues to be investigated, its hallmark pathologies (i.e., oxidative stress, tau protein aggregation, and amyloid-beta (Aβ) accumulation) have long been established.4,5 The amyloid hypothesis, proposed more than three decades ago, suggests that Aβ aggregation triggers a neurotoxic cascade.6,7 Aβ peptides arise from the proteolytic processing of the amyloid precursor protein (APP) and range from 38–43 residues in length. The gene discussed is APP; the disease is Alzheimer disease.