Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease
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 act...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/952375 |
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| _version_ | 1832561448411201536 |
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| author | Sandeep Vasant More Hemant Kumar In Su Kim Soo-Yeol Song Dong-Kug Choi |
| author_facet | Sandeep Vasant More Hemant Kumar In Su Kim Soo-Yeol Song Dong-Kug Choi |
| author_sort | Sandeep Vasant More |
| collection | DOAJ |
| description | 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-1β), 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. |
| format | Article |
| id | doaj-art-aa35de788e5e410ea13a4efc9743bfed |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-aa35de788e5e410ea13a4efc9743bfed2025-02-03T01:24:56ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/952375952375Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s DiseaseSandeep Vasant More0Hemant Kumar1In Su Kim2Soo-Yeol Song3Dong-Kug Choi4Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of KoreaDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of KoreaDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of KoreaDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of KoreaDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of KoreaNeuroinflammation 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-1β), 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.http://dx.doi.org/10.1155/2013/952375 |
| spellingShingle | Sandeep Vasant More Hemant Kumar In Su Kim Soo-Yeol Song Dong-Kug Choi Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease Mediators of Inflammation |
| title | Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease |
| title_full | Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease |
| title_fullStr | Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease |
| title_full_unstemmed | Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease |
| title_short | Cellular and Molecular Mediators of Neuroinflammation in the Pathogenesis of Parkinson’s Disease |
| title_sort | cellular and molecular mediators of neuroinflammation in the pathogenesis of parkinson s disease |
| url | http://dx.doi.org/10.1155/2013/952375 |
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