AD is commonly characterized by the presence of senile plaques, large extracellular aggregates of fibrillary amyloid-β peptide (Aβ), originated by the abnormal cleavage of amyloid precursor protein where the sequential cleavage of amyloid precursor protein by β- and γ-secretase produces the neurotoxic Aβ peptide (Scheuner et al., 1996; Ertekin-Taner, 2007). Here, APP is linked to Alzheimer disease.