KONTRIBUSI INFLAMASI TERHADAP PATOGENESIS PENYAKIT PARKINSON

Parkinson’s disease is one of neurodegenerative diseases which is the second most common afterAlzheimer’s disease in the world. It is a chronic disease with selective loss of dopaminergic neurons withinthe substantia nigra (SN) pars compacta (pc) of the midbrain. The disease represents a complex interactionbetween the inherent vulnerability of the nigrostriatal dopaminergic system, a possible geneticpredisposition, and exposures to environmental toxins including inflammatory triggers. Until now, the exactcause of Parkinson’s disease remains uncertain, but recent studies suggest neuroinflammation andmicroglia activation play important roles in Parkinson’s disease pathogenesis. Evidence now suggest thatchronic neuroinflammation and systemic inflammation are consistently associated with the patophysiologyof Parkinson’s disease. Activated microglia and increased level of pro-inflammatory cytokine such as TumorNecrosis Factor (TNF)-α, interleukin (IL)-2, IL-6, RANTES, Reactive Oxygen Species (ROS) and NitricOxide (NO) have been reported from Parkinson’s disease patients and in animal models of Parkinson’sdisease. The blood brain barrier permeability dysfunction is also a contributing factor to the pathology ofthis disease. In this review, we discuss about neuronal cell pathology in Parkinson’s disease, its possiblerelationship with neuroinflammation and systemic inflammation, blood brain barrier disfunction and proinflammatory cytokine released during the disease’s progressivity. Lastly, we also review theepidemiological data suggest about the inflammation and the increased risk of Parkinson’s disease. Moreresearch are needed to undercover the role of inflammation in Parkinson’s disease. With a betterunderstanding about the relationship between inflammation and Parkinson’s disease cross-talk, the brightfuture with the possibility of specific immunomodulatory drugs play a role to limit a progressivity ofParkinson’s disease is no longer just a dream.