Whether the cause is genetically familial or multifactorial late-onset AD, the main neuropathological features are the extensive extracellular deposition of insoluble amyloid Aβ formed by the hydrolysis of APP by β and γ hydrolases and the intracellular neurofibrillary tangles (NFTs) formed by hyperphosphorylated tau protein [33,34]. Here, APP is linked to Alzheimer disease.