The two cardinal features of AD pathology speculated to be the potential targets of disease-modifying drugs are β-amyloid (Aβ), a product of aberrant amyloid precursor protein (APP) leading to production of extracellular Aβ plaques, and NFT arising from hyperphosphorylation of tau, a microtubule-associated protein (Giacobini and Becker, 2007). The gene discussed is APP; the disease is Alzheimer disease.