CAMK2G and early-onset autosomal dominant Alzheimer disease: Furthermore, redox-mediated NMDAR hypofunction, and the interaction of CaMKII and GluN2B are thought to provide a link between altered synaptic plasticity and cognitive deficits for a range of illnesses including Alzheimer’s disease, depression, schizophrenia, and impaired episodic memory during aging [4,8,10,41,42,65,66].