APP and Alzheimer disease: Traditionally, the most important pathomechanism of AD is hypothesized to be the amyloid-β (Aβ) cascade, in which the brain harbors abnormal accumulation of Aβ cleaved from amyloid precursor protein (APP) into toxic extracellular plaques; another pathomechanism is the intracellular accumulation of neurofibrillary tangles made of hyperphosphorylated and misfolded tau protein [2].