We showed a major role of the local brain RAS in neuroinflammation and dopaminergic degeneration in Parkinson’s disease (PD) models, including classical 6-hydroxydopamine (6-OHDA)- and MPTP-induced neurotoxic PD models in rats and mice, showing that AngII, via AT1 receptors, increases the dopaminergic degeneration process by amplifying the inflammatory response and intraneuronal levels of oxidative stress, and that microglial cells play a major role in this process, which is inhibited by treatment AT1 receptor antagonists [15,16]. This evidence concerns the gene AGTR1 and Parkinson disease.