To date, the central neuropathological hallmarks noticed in AD are extracellular amyloid beta (Aβ) plaques, a consequence of aberrant transmembrane amyloid precursor protein (APP) cleavage, accumulation of large intracellular quantities of neurofibrillary tangles, cerebral amyloid angiopathy, glial cell dysfunction, synaptic, and neuronal injury [10,11]. Here, APP is linked to Alzheimer disease.