Based on above, TES neuroprotection against stroke in aging appears to be mediated by several mechanisms including inhibition of production of oxidant molecules, enhancing the enzymatic antioxidant capacity of the brain, activation of PI3K/AKT pathway and enhancing cell survival, inhibition of pro-apoptotic protein through AR-dependent MAPK/ERK pathway, as well as improvement of brain neuronal and BBB integrities. This evidence concerns the gene AKT1 and stroke disorder.