Consistent with this, our optogenetic technique that selectively stimulated CaMKII–CHR2-expressing neurons in the DG of the bilateral hippocampus improved working memory and short-term memory, altered neuroinflammation, attenuated excitotoxicity induced by Aβ, and exerted neuroprotective effects in our mouse model of AD. The gene discussed is CAMK2G; the disease is Alzheimer disease.