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Review
. 2013:2013:952375.
doi: 10.1155/2013/952375. Epub 2013 Jun 27.

Cellular and molecular mediators of neuroinflammation in the pathogenesis of Parkinson's disease

Sandeep Vasant More  1 , Hemant Kumar, In Su Kim, Soo-Yeol Song, Dong-Kug Choi
Affiliations
Review

Cellular and molecular mediators of neuroinflammation in the pathogenesis of Parkinson's disease

Sandeep Vasant More et al. Mediators Inflamm. 2013.

Abstract

Neuroinflammation is a host-defense mechanism associated with restoration of normal structure and function of the brain and neutralization of an insult. Increasing neuropathological and biochemical evidence from the brains of individuals with Parkinson's disease (PD) provides strong evidence for activation of neuroinflammatory pathways. Microglia, the resident innate immune cells, may play a major role in the inflammatory process of the diseased brain of patients with PD. Although microglia forms the first line of defense for the neural parenchyma, uncontrolled activation of microglia may directly affect neurons by releasing various molecular mediators such as inflammatory cytokines (tumor necrosis factor- α , interleukin [IL]-6, and IL-1 β ), nitric oxide, prostaglandin E2, and reactive oxygen and nitrogen species. Moreover, recent studies have reported that activated microglia phagocytose not only damaged cell debris but also intact neighboring cells. This phenomenon further supports their active participation in self-enduring neuronal damage cycles. As the relationship between PD and neuroinflammation is being studied, there is a realization that both cellular and molecular mediators are most likely assisting pathological processes leading to disease progression. Here, we discuss mediators of neuroinflammation, which are known activators released from damaged parenchyma of the brain and result in neuronal degeneration in patients with PD.

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Figures

Figure 1
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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