According to the amyloid β (Aβ) hypothesis, the underlying pathogenesis of AD is an accumulation of Aβ that results from abnormal cleavage of amyloid precursor protein (APP) by γ‐secretase, followed by abnormal phosphorylation and accumulation of tau (Hardy & Allsop, 1991; Hardy & Selkoe, 2002). Here, APP is linked to Alzheimer disease.