Review Article

Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease

Figure 1

Microglial and astroglial cells become activated during the pathogenesis of Parkinson’s disease under the influence of various proinflammatory triggers, including α-synuclein, the complement system, and cytokines released from infiltrated T cells. Activated microglial and astroglial cells further release various neuroinflammatory mediators, including NO, COX-2, IFN-γ, TNF-α, IL-1β & IL-6, chemokines including MCP-1α, MIP-α and CXCL-8, and MAC which have deleterious effect on neuronal survival. Abbreviations: NO: nitric oxide, COX-2: cyclooxygenase, INF-γ: interferon-γ, TNF-α: tumor necrosis factor-α, IL-1β: interleukin-1β, IL-6: interleukin-6, MCP-1α: monocyte chemotactic protein-1, MIP-α: microphage inflammatory protein, IL-8: interleukin-8, MAC: membrane attack complex, α-syn: α-synuclein, MMP: matrix metalloprotein, BBB: blood brain barrier, C3a: complement component 3a, and C4a: complement component 4a.
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