Moreover, NO was neuroprotective in various animal models of Parkinson Disease, after oxygen-glucose deprivation or cerebral ischemia/reperfusion injury and this effect depended on a reduction in reactive oxygen species and protein S-nitrosylation in brain mitochondria50,51, while in a pharmacological study, neuroprotection occurred in a PI3K/Akt dependent manner52. This evidence concerns the gene AKT1 and Cerebral ischemia.