Neuroinflammatory processes in Parkinson's disease
Identifieur interne : 001220 ( Istex/Corpus ); précédent : 001219; suivant : 001221Neuroinflammatory processes in Parkinson's disease
Auteurs : Stephane Hunot ; E. C. HirschSource :
- Annals of Neurology [ 0364-5134 ] ; 2003.
Abstract
Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60
Url:
DOI: 10.1002/ana.10481
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title><author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stephane" last="Hunot">Stephane Hunot</name><affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name><affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</idno><date when="2003" year="2003">2003</date><idno type="doi">10.1002/ana.10481</idno><idno type="url">https://api.istex.fr/document/BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001220</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001220</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title><author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stephane" last="Hunot">Stephane Hunot</name><affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name><affiliation><mods:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2003">2003</date><biblScope unit="volume">53</biblScope><biblScope unit="issue">S3</biblScope><biblScope unit="supplement">3</biblScope><biblScope unit="page" from="S49">S49</biblScope><biblScope unit="page" to="S60">S60</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</idno><idno type="DOI">10.1002/ana.10481</idno><idno type="ArticleID">ANA10481</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Stephane Hunot PhD</name><affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, Paris, France</json:string><json:string>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>E. C. Hirsch PhD</name><affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, Paris, France</json:string></affiliations></json:item></author><articleId><json:string>ANA10481</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. 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Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & 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Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><availability><p>Copyright © 2003 Wiley‐Liss, Inc.</p></availability><date>2003</date></publicationStmt><notesStmt><note>INSERM</note><note>CNRS</note><note>National Parkinson Foundation (Miami, FL)</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title><author xml:id="author-1"><persName><forename type="first">Stephane</forename><surname>Hunot</surname></persName><roleName type="degree">PhD</roleName><affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation><affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">E. C.</forename><surname>Hirsch</surname></persName><roleName type="degree">PhD</roleName><affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2003"></date><biblScope unit="volume">53</biblScope><biblScope unit="issue">S3</biblScope><biblScope unit="supplement">3</biblScope><biblScope unit="page" from="S49">S49</biblScope><biblScope unit="page" to="S60">S60</biblScope></imprint></monogr><idno type="istex">BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</idno><idno type="DOI">10.1002/ana.10481</idno><idno type="ArticleID">ANA10481</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Research Articles</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8249</doi><issn type="print">0364-5134</issn><issn type="electronic">1531-8249</issn><idGroup><id type="product" value="ANA"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="ANNALS OF NEUROLOGY">Annals of Neurology</title><title type="subtitle">Official Journal of the American Neurological Association and the Child Neurology Society</title><title type="short">Ann Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="45"><doi origin="wiley" registered="yes">10.1002/ana.v53:3+</doi><titleGroup><title type="supplementTitle">Neurogeneration and Prospects for Neuroprotection and Rescue in Parkinson's Disease</title></titleGroup><numberingGroup><numbering type="journalVolume" number="53">53</numbering><numbering type="journalIssue">S3</numbering><numbering type="supplement" number="3">3</numbering></numberingGroup><coverDate startDate="2003">2003</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="6" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ana.10481</doi><idGroup><id type="unit" value="ANA10481"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="articleCategory">Research Articles</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2003 Wiley‐Liss, Inc.</copyright><eventGroup><event type="firstOnline" date="2003-03-24"></event><event type="publishedOnlineFinalForm" date="2003-03-24"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.1 mode:FullText source:FullText result:FullText" date="2010-02-23"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">S49</numbering><numbering type="pageLast">S60</numbering></numberingGroup><correspondenceTo>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA10481.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="83"></count><count type="wordTotal" number="8552"></count></countGroup><titleGroup><title type="main" xml:lang="en">Neuroinflammatory processes in Parkinson's disease</title><title type="short" xml:lang="en">Neuroinflammatory Process in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Stephane</givenNames><familyName>Hunot</familyName><degrees>PhD</degrees></personName><contactDetails><email>hunot@ccr.jussieu.fr</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>E. C.</givenNames><familyName>Hirsch</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>INSERM</fundingAgency></fundingInfo><fundingInfo><fundingAgency>CNRS</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Parkinson Foundation (Miami, FL)</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neuroinflammatory processes in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Neuroinflammatory Process in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Neuroinflammatory processes in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Stephane</namePart><namePart type="family">Hunot</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation><affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E. C.</namePart><namePart type="family">Hirsch</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2003</dateIssued><copyrightDate encoding="w3cdtf">2003</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">3</extent><extent unit="references">83</extent><extent unit="words">8552</extent></physicalDescription><abstract lang="en">Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory‐associated factors such as cyclooxygenase‐2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD. Ann Neurol 2003;53 (suppl 3):S49–S60</abstract><note type="funding">INSERM</note><note type="funding">CNRS</note><note type="funding">National Parkinson Foundation (Miami, FL)</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Research Articles</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>53</number></detail><detail type="issue"><caption>no.</caption><number>S3</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>3</number></detail><extent unit="pages"><start>S49</start><end>S60</end><total>12</total></extent></part></relatedItem><identifier type="istex">BF5A7E3CCACFF44C9861F7B07E7911FF2BF80A88</identifier><identifier type="DOI">10.1002/ana.10481</identifier><identifier type="ArticleID">ANA10481</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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