Opazo et al. (2018) showed that oligomeric forms of Aβ peptide engage in synaptic metaplasticity via aberrant activation of CaMKII, mediated through GluN2B-containing NMDARs, which leads to LTP deficits and destabilization of AMPARs in the early stages of AD. This evidence concerns the gene CAMK2G and Alzheimer disease.