CAMK2G and Alzheimer disease: We also extend our research on synaptic Ca2+ signalling to the downstream CaMKII state transition to investigate the disturbances from alterations in synaptic NMDAR in the emergence of LTP in AD: we integrate the Ca2+ model with a state transition model of CaMKII to study the subunit-specific roles of NMDAR in the postsynaptic response and the formation of NMDAR-mediated LTP.