It has also been reported that one of the earliest biological manifestations of Alzheimer’s dementia is a decrease in AMPA-type receptors and impaired synaptic plasticity [67,68], and a reduction of autophosphorylation of CaMKII at threonine 286 in the frontal cortex and hippocampus of Alzheimer’s disease brains is a key contributor to synaptic dysfunction, neurodegeneration, and memory impairment [44,69]. Here, CAMK2G is linked to memory impairment.