The cause of Parkinson's disease (PD) remains elusive in both patients and experimental models of PD in mice and monkeys present pathological changes with the classical features of chronic inflammation mounted by activated microglia. Microglia mediates innate immune responses to invading pathogens by secreting cytokines, chemokines, prostaglandins, reactive oxygen and nitrogen species, and growth factors. However, even if some of these factors aid the brain repair processes by its neuroprotective and trophic activities, others factors can starts apoptotic cascades in a vicious circle. We have studied some endogenous regulatory processes that determine inflammation and microglial actions in pathological states in parkinsonian monkeys chronically intoxicated by MPTP. Together, our data indicate that: i) microglial reactivity and its deregulation in PD could lead to sustained inflammation-mediated dopamine neurons injury, and ii) how some anti-inflammatory and anti-oxidant drugs could be potential agents for the treatment of PD.