Microglial activation mediates neurodegeneration related to oligodendroglial α‐synucleinopathy: Implications for multiple system atrophy
Identifieur interne : 001D93 ( Istex/Corpus ); précédent : 001D92; suivant : 001D94Microglial activation mediates neurodegeneration related to oligodendroglial α‐synucleinopathy: Implications for multiple system atrophy
Auteurs : Nadia Stefanova ; Markus Reindl ; Manuela Neumann ; Philipp J. Kahle ; Werner Poewe ; Gregor K. WenningSource :
- Movement Disorders [ 0885-3185 ] ; 2007-11-15.
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Abstract
The role of microglial activation in multiple system atrophy (MSA) was investigated in a transgenic mouse model featuring oligodendroglial α‐synuclein inclusions and loss of midbrain dopaminergic neurons by means of histopathology and morphometric analysis. Our findings demonstrate early progressive microglial activation in substantia nigra pars compacta (SNc) associated with increased expression of iNOS and correlating with dopaminergic neuronal loss. Suppression of microglial activation by early long‐term minocycline treatment protected dopaminergic SNc neurons. The results suggest that oligodendroglial overexpression of α‐synuclein may induce neuroinflammation related to nitrosive stress which is likely to contribute to neurodegeneration in MSA. Further, we detected increased toll‐like receptor 4 immunoreactivity in both transgenic mice and MSA brains indicating a possible signaling pathway in MSA which needs to be further studied as a candidate target for neuroprotective interventions. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21671
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ISTEX:9DAFFB13F2D836A08E6DF45D7B51C27BD3C79A73Le document en format XML
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Our findings demonstrate early progressive microglial activation in substantia nigra pars compacta (SNc) associated with increased expression of iNOS and correlating with dopaminergic neuronal loss. Suppression of microglial activation by early long‐term minocycline treatment protected dopaminergic SNc neurons. The results suggest that oligodendroglial overexpression of α‐synuclein may induce neuroinflammation related to nitrosive stress which is likely to contribute to neurodegeneration in MSA. Further, we detected increased toll‐like receptor 4 immunoreactivity in both transgenic mice and MSA brains indicating a possible signaling pathway in MSA which needs to be further studied as a candidate target for neuroprotective interventions. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Nadia Stefanova MD, PhD</name><affiliations><json:string>Clinical Neurobiology Unit, Neurodegeneration Research Laboratory, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Markus Reindl PhD</name><affiliations><json:string>Clinical Neurobiology Unit, Neurodegeneration Research Laboratory, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Manuela Neumann MD</name><affiliations><json:string>Center for Neuropathology and Prion Research Brain Bank, University of Munich, Germany</json:string></affiliations></json:item><json:item><name>Philipp J. 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Foundation</fundingAgency><fundingNumber>P16128‐B05</fundingNumber><fundingNumber>P19989‐B05</fundingNumber></fundingInfo><fundingInfo><fundingAgency>German Federal Ministry of Education and Research (“Brain‐Net”)</fundingAgency><fundingNumber>01GI0299</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The role of microglial activation in multiple system atrophy (MSA) was investigated in a transgenic mouse model featuring oligodendroglial α‐synuclein inclusions and loss of midbrain dopaminergic neurons by means of histopathology and morphometric analysis. Our findings demonstrate early progressive microglial activation in substantia nigra pars compacta (SNc) associated with increased expression of iNOS and correlating with dopaminergic neuronal loss. Suppression of microglial activation by early long‐term minocycline treatment protected dopaminergic SNc neurons. The results suggest that oligodendroglial overexpression of α‐synuclein may induce neuroinflammation related to nitrosive stress which is likely to contribute to neurodegeneration in MSA. Further, we detected increased toll‐like receptor 4 immunoreactivity in both transgenic mice and MSA brains indicating a possible signaling pathway in MSA which needs to be further studied as a candidate target for neuroprotective interventions. © 2007 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Microglial activation mediates neurodegeneration related to oligodendroglial α‐synucleinopathy: Implications for multiple system atrophy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Neuroinflammation and MSA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Microglial activation mediates neurodegeneration related to oligodendroglial α‐synucleinopathy: Implications for multiple system atrophy</title></titleInfo><name type="personal"><namePart type="given">Nadia</namePart><namePart type="family">Stefanova</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Neurobiology Unit, Neurodegeneration Research Laboratory, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Markus</namePart><namePart type="family">Reindl</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Clinical Neurobiology Unit, Neurodegeneration Research Laboratory, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Manuela</namePart><namePart type="family">Neumann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Center for Neuropathology and Prion Research Brain Bank, University of Munich, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philipp J.</namePart><namePart type="family">Kahle</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Laboratory of Functional Neurogenetics, Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University Clinics Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Clinical Neurobiology Unit, Neurodegeneration Research Laboratory, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregor K.</namePart><namePart type="family">Wenning</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Neurobiology Unit, Neurodegeneration Research Laboratory, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</affiliation><description>Correspondence: Department of Neurology, Innsbruck Medical University, Anichstrasse 35, A‐6020 Innsbruck, Austria</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-11-15</dateIssued><dateCaptured encoding="w3cdtf">2007-03-30</dateCaptured><dateValid encoding="w3cdtf">2007-06-28</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="tables">1</extent><extent unit="references">31</extent><extent unit="words">4377</extent></physicalDescription><abstract lang="en">The role of microglial activation in multiple system atrophy (MSA) was investigated in a transgenic mouse model featuring oligodendroglial α‐synuclein inclusions and loss of midbrain dopaminergic neurons by means of histopathology and morphometric analysis. Our findings demonstrate early progressive microglial activation in substantia nigra pars compacta (SNc) associated with increased expression of iNOS and correlating with dopaminergic neuronal loss. Suppression of microglial activation by early long‐term minocycline treatment protected dopaminergic SNc neurons. The results suggest that oligodendroglial overexpression of α‐synuclein may induce neuroinflammation related to nitrosive stress which is likely to contribute to neurodegeneration in MSA. Further, we detected increased toll‐like receptor 4 immunoreactivity in both transgenic mice and MSA brains indicating a possible signaling pathway in MSA which needs to be further studied as a candidate target for neuroprotective interventions. © 2007 Movement Disorder Society</abstract><note type="funding">Austrian Science Foundation - No. P16128‐B05; No. P19989‐B05; </note><note type="funding">German Federal Ministry of Education and Research (“Brain‐Net”) - No. 01GI0299; </note><subject lang="en"><genre>Keywords</genre><topic>α‐synuclein</topic><topic>multiple system atrophy</topic><topic>microglial activation</topic><topic>transgenic mouse</topic><topic>neurodegeneration</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2196</start><end>2203</end><total>8</total></extent></part></relatedItem><identifier type="istex">9DAFFB13F2D836A08E6DF45D7B51C27BD3C79A73</identifier><identifier type="DOI">10.1002/mds.21671</identifier><identifier type="ArticleID">MDS21671</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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