The hallmark neuropathologic characteristic of AD is abnormal extracellular protein accumulation in the brain, notably the extracellular deposition of amyloid-β (Aβ) peptide generated from the improper cleavage of amyloid precursor protein (APP) that gives rise to Aβ monomers that aggregate into oligomeric Aβ fibrils and plaques, and intraneuronal neurofibrillary tangles (NF) comprised largely of hyperphosphorylated tau. This evidence concerns the gene APP and Alzheimer disease.