In addition, we do not know whether these AKAP-mediated regulatory mechanisms also control CP-AMPAR mediated plasticity in the hippocampus during pathophysiological states, such as during ischemia and with amyloid-beta exposure during Alzheimer’s disease (Liu and Zukin, 2007; Whitcomb et al., 2015), or in other brain regions where changes in CP-AMPAR synaptic incorporation have been observed, such as in the nucleus accumbens and ventral tegmental area in drug addiction models and in the basolateral amygdala in fear extinction learning (Clem and Huganir, 2010; Wolf and Tseng, 2012). This evidence concerns the gene CP and Alzheimer disease.