The prevailing theory regarding the cause of AD is the amyloid cascade hypothesis, which posits that overproduction of Aβ from amyloid precursor protein (APP) initiates a series of events, including synaptic dysfunction, microglial and astrocytic activation and hyperphosphorylation of tau, which culminates in widespread neuronal death and neurodegeneration (Hardy and Selkoe, 2002). The gene discussed is APP; the disease is Alzheimer disease.