| Neurodegeneration and Inflammation in Parkinson's disease. | |
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MedLine Citation:
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PMID: 22166436 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Parkinson's disease (PD) is characterized by the progressive degeneration of dopamine (DA) neurons of the substantia nigra pars compacta (SNpc) accompanied by a buildup of proteinaceous aggregates termed Lewy bodies (LB). In addition to protein aggregation and the loss of DA signaling, PD is also characterized by an active immune response. T-cell infiltration accompanies activated microglial and astrocytic accumulation in and around the SNpc. Although potentially beneficial, microglial activation is most likely responsible for furthering disease pathology and DA neuron degeneration through the release of harmful substances such as pro-inflammatory cytokines, reactive oxidative species and reactive nitrogen species. Activation of the NF-κB death pathway has been shown to occur following microglial activation related release of Cox-2, IL-1β, and Toll-like receptor activation, resulting in increased degeneration of DA neurons of the SNpc. Blockade of microglial activation can lead to DA neuron protection in animal models of PD; however, clinical application of anti-inflammatory drugs has not yielded similar benefits. Future therapeutic designs must take into account the multifactorial nature of PD, including the varied roles of the adaptive and innate immune responses. |
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Authors:
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Sudarshan Phani; John D Loike; Serge Przedborski |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Parkinsonism & related disorders Volume: 18 Suppl 1 ISSN: 1873-5126 ISO Abbreviation: Parkinsonism Relat. Disord. Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2011-12-14 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9513583 Medline TA: Parkinsonism Relat Disord Country: England |
Other Details:
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Languages: eng Pagination: S207-9 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Neurology, Pathology and Cell Biology, Columbia University, New York, NY, USA; Center for Motor Neuron Biology and Disease, Columbia University, New York, NY, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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