title: Neuroinflammation in Parkinson's disease.
abstract: Both epidemiological and genetic studies support a role of neuroinflammation in the pathophysiology of Parkinson's disease (PD). Furthermore, post mortem studies confirm the involvement of innate as well as adaptive immunity in the affected brain regions in patients with PD. Indeed, activated microglial cells and T lymphocytes have been detected in the substantia nigra of patients concomitantly with an increased expression of pro-inflammatory mediators. Preclinical investigations conducted in various animal models of PD indicate that inflammatory processes are instrumental in neuronal cell death even though they are unlikely to be a primary cause for neuronal loss. Neuroinflammatory processes in PD are rather involved in self-perpetuating deleterious events that lead to protracted neuronal degeneration. In line with this, recent data indicate that glucocorticoid receptors are important in curtailing microglial reactivity, and deregulation in their activity in PD could lead to sustained inflammation-mediated degeneration. Altogether, neuroinflammatory processes might represent a target for neuroprotection in PD.
authors.affiliation: INSERM, UMR_S975, CRicm, Experimental Therapeutics of neurodegeneration, F-75013, Paris, France. etienne.hirsch@upmc.fr
authors.forename: Etienne C
authors.initials: EC
authors.lastname: Hirsch
authors.forename: Sheela
authors.initials: S
authors.lastname: Vyas
authors.forename: Stéphane
authors.initials: S
authors.lastname: Hunot
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D009410:Nerve Degeneration / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D010300:Parkinson Disease / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal