Consistent with this, our data reveal gliosis-mediated neuroinflammation and enhancement in IL-17 and IFN-γ, whereas CA reduced their production, and prevented MPTP-mediated microgliosis as well as astrogliosis along with increased BDNF, the improvement in DA neuronal survival and motor function, suggesting that CA acted as an immunological mediator of the peripheral immune system and inhibited neuroinflammation in PD. This evidence concerns the gene IFNG and Parkinson disease.