Fig. 1

Diagrammatic representation of inflammatory mechanisms involved in PD pathogenesis. Microglia become activated M1 phenotype in PD under pathological conditions such as protein aggregation, gene mutations, environmental factors and cytokines released from infiltrated T cells. The pro-inflammatory mediators from M1 microglia activate astrocytes leading to elevated production of proinflammatory factors, nitric oxide and superoxide radical, contributing to degeneration of DA neurons. The molecules released from degenerative DA neurons can further cause activation of glia and enhanced inflammatory response. At certain stage of PD, subpopulation of microglia may become activated M2 phenotype releasing anti-inflammatory factors, including TGF-β, and exert a neuroprotective effect in PD