The interest in studying neuroimmune interactions is increasing in the scientific community, and for many researchers, immunity is becoming a crucial factor in the understanding of the physiology of the normal brain as well as the biology underlying neurodegenerative diseases. Mounting data over the last two decades point toward immune and inflammatory alterations as important mediators of the progressive dopaminergic degeneration in Parkinson’s disease. The purpose of this review is to address, under a historical perspective, as well as in the light of recent reports, the glial-mediated inflammatory and immune responses that occur in Parkinsonism. In line with this, this review also evaluates and highlights available anti-inflammatory drugs and putative targets for Parkinson’s disease therapy for the near future. 1. Introduction After many decades of research, the cause of idiopathic Parkinson’s disease (PD) remains unknown. A number of hypotheses have been put forward to explain the origin of the disease. However, the understanding of the mechanisms underlying PD remains inconclusive. The trigger of dopaminergic degeneration seems to be multifactorial and, therefore, affected by both endogenous and environmental elements. In the light of recent epidemiological, genetic, and experimental studies, inflammation and immune responses are considered as important mediators of dopaminergic degeneration. Large population studies have come to conclude that individuals taking nonsteroidal anti-inflammatory drugs (NSAIDs) have less risk of suffering idiopathic PD, which suggest that anti-inflammatory drugs may be a promising disease-modifying treatment for Parkinsonian patients [1–4]. Important genetic studies have shown an increase of polymorphisms of the human leukocyte antigen (HLA)-DR type gene in sporadic PD, indicating an immune/inflammatory-related component of the disease [5, 6]. Despite the extended basic research performed in experimental models of PD and the positive outcome of a wide range of tested anti- inflammatory drugs, the translational aspect toward a neuroimmune-modifying therapy in PD has been rather slow. In recent years, some pharmacological companies have taken steps towards the development of therapeutic programs. New trial phases have recently been started to implement anti-inflammatory treatments for the near future. There are a number of clinical trials, essentially focused on monitoring the evolution of the inflammatory response in the brain of PD patients in vivo, using potential imaging biomarkers in the course of dopaminergic
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