The immunohistochemical demonstration of reactive microglia and activated complement components suggests that chronic inflammation occurs in affected brain regions in Parkinson's disease (PD). Evidence from humans and monkeys exposed to MPTP indicates this inflammation may persist many years after the initial stimulus has disappeared. Chronic inflammation can damage host cells. Reports in the literature indicate that antiinflammatory agents inhibit dopaminergic cell death in animal models of PD, and there is one epidemiological report that their use significantly diminishes the risk of PD in humans. There is a marked elevation in the mRNA levels for complement proteins and markers of activated microglia in affected regions in PD. The upregulation appears greater than that found in inflamed arthritic joints. These data support the hypothesis that chronic inflammation may play an important role, if secondary, in the pathogenesis of PD.