Similarly, in Alzheimer’s disease (AD), excitotoxicity, and ischemic stroke models, NPY2R activation—along with a lesser contribution from NPY5R—attenuated caspase-3 activation, suppressed glutamate release, increased AKT phosphorylation, and preserved neuronal integrity [33, 101, 102]. The gene discussed is AKT1; the disease is Alzheimer disease.