Treatment of cortical neurons with Aβ fibrils promotes ER Ca2+ release through RyR and IP3R channels, inducing ER stress, oxidative stress, and cell death (Ferreiro et al., 2008; Resende et al., 2008), while enhanced RyR recruitment contributes to Ca2+ disruptions in young, adult, and aged AD mice (Stutzmann et al., 2006), an effect of particular importance in dendritic spines (Goussakov et al., 2010). The gene discussed is ITPR1; the disease is Alzheimer disease.