The main pathological hallmark of AD is the extracellular senile plaques, formed by the deposition of amyloid-β (Aβ) peptides, which derive from the sequential enzymatic cleavage of amyloid precursor protein (APP) by the β-secretase and γ-secretase (Bossy-Wetzel et al., 2004; Baranello et al., 2015). Here, APP is linked to Alzheimer disease.