A large body of evidence supports that the accumulation of intracellular Aβ42, a proteolytic cleavage of amyloid precursor protein (APP) by β-site APP-cleaving enzyme 1 (BACE1), which plays a central role in AD pathogenesis by processing APP to Aβ, is a critical event in the pathogenic mechanism of AD, and reducing the accumulation of Aβ can mitigate the progression of AD69–71. Here, BACE1 is linked to Alzheimer disease.