Alzheimer’s disease, the most common neurodegenerative disorder, is pathogenically linked to the accumulation of association-prone amyloid-β (Aβ) peptides originating from the amyloidogenic cleavage of the β-amyloid precursor protein (APP), a non-amyloidogenic, physiological cellular protein, through sequential proteolysis mediated by β- and γ-secretases residing in lipid rafts of the plasma membrane and in endolysosomal compartments. Here, APP is linked to early-onset autosomal dominant Alzheimer disease.