Abnormal accumulation of amyloid β oligomers (AβO) has been implicated in the pathogenesis of early stage AD (Hardy and Selkoe 2002; Lambert et al. 1998; Lesne et al. 2006; McLean et al. 1999; Walsh and Selkoe 2004), causing synaptic dysfunctions (Lacor et al. 2004; Shankar et al. 2007, 2008; Hsieh et al. 2006; Kamenetz et al. 2003) including impairments to synaptic plasticity (Lambert et al. 1998; Walsh and Selkoe 2004; Walsh et al. 2002) and ultimately neuronal death (Alberdi et al. 2010; De Felice et al. 2007; Decker et al. 2010). The gene discussed is ABO; the disease is Alzheimer disease.