Since calcium entry is pathologically increased in AD due to the effect of Aβ oligomers (oAβ) on NMDA receptors [11], and oxidative stress is one the main neurotoxic mechanisms of Aβ [11,12,13], here we have aimed the study of the post-translational modifications of neuronal CaMKIIα due to oAβ and the effects on its activity. This evidence concerns the gene CAMK2A and Alzheimer disease.