Pathogenesis of Parkinson's disease
Identifieur interne : 000E03 ( Istex/Corpus ); précédent : 000E02; suivant : 000E04Pathogenesis of Parkinson's disease
Auteurs : Etienne C. Hirsch ; Peter Jenner ; Serge PrzedborskiSource :
- Movement Disorders [ 0885-3185 ] ; 2013-01.
Abstract
Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. Currently, it is believed that the neurodegenerative process in Parkinson's disease is a combination of both cell‐autonomous and non‐cell‐autonomous mechanisms. Proposed cell‐autonomous mechanisms include alterations in mitochondrial bioenergetics, dysregulation of calcium homeostasis, and impaired turnover of mitochondria. As for the proposed non‐cell‐autonomous mechanisms, they involve prion‐like behavior of misfolded proteins and neuroinflammation. This suggests that cell death in Parkinson's disease is caused by a multifactorial cascade of pathogenic events and argues that effective neuroprotective therapy for Parkinson's disease may have to rely on multiple drug interventions. © 2013 Movement Disorder Society
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DOI: 10.1002/mds.25032
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ISTEX:169622838E7D6D3DB3B55A5455A3D2869BCB4F91Le document en format XML
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Hirsch</name><affiliation><mods:affiliation>Université Pierre et Marie Curie–Paris 06, Centre de Recherche de l'Institut du Cerveau et de la Moëlle Épinière, Hôpital de la Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité Mixte de Recherche U975, Institut National de la Santé et de la Recherche Médicale, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité Mixte de Recherche 7225, Centre National de la Recherche Scientifique, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, Institute of Pharmaceutical Sciences, School of Biomedical Sciences, King's College, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Przedborski, Serge" sort="Przedborski, Serge" uniqKey="Przedborski S" first="Serge" last="Przedborski">Serge Przedborski</name><affiliation><mods:affiliation>Department of Neurology, Department of Pathology and Cell Biology, and the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: sp30@columbia.edu</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:169622838E7D6D3DB3B55A5455A3D2869BCB4F91</idno><date when="2013" year="2013">2013</date><idno type="doi">10.1002/mds.25032</idno><idno type="url">https://api.istex.fr/document/169622838E7D6D3DB3B55A5455A3D2869BCB4F91/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000E03</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000E03</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Pathogenesis of Parkinson's disease</title><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name><affiliation><mods:affiliation>Université Pierre et Marie Curie–Paris 06, Centre de Recherche de l'Institut du Cerveau et de la Moëlle Épinière, Hôpital de la Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité Mixte de Recherche U975, Institut National de la Santé et de la Recherche Médicale, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité Mixte de Recherche 7225, Centre National de la Recherche Scientifique, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, Institute of Pharmaceutical Sciences, School of Biomedical Sciences, King's College, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Przedborski, Serge" sort="Przedborski, Serge" uniqKey="Przedborski S" first="Serge" last="Przedborski">Serge Przedborski</name><affiliation><mods:affiliation>Department of Neurology, Department of Pathology and Cell Biology, and the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: sp30@columbia.edu</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov Disord</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><date type="published" when="2013-01">2013-01</date><biblScope unit="volume">28</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="24">24</biblScope><biblScope unit="page" to="30">30</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">169622838E7D6D3DB3B55A5455A3D2869BCB4F91</idno><idno type="DOI">10.1002/mds.25032</idno><idno type="ArticleID">MDS25032</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. Currently, it is believed that the neurodegenerative process in Parkinson's disease is a combination of both cell‐autonomous and non‐cell‐autonomous mechanisms. Proposed cell‐autonomous mechanisms include alterations in mitochondrial bioenergetics, dysregulation of calcium homeostasis, and impaired turnover of mitochondria. As for the proposed non‐cell‐autonomous mechanisms, they involve prion‐like behavior of misfolded proteins and neuroinflammation. This suggests that cell death in Parkinson's disease is caused by a multifactorial cascade of pathogenic events and argues that effective neuroprotective therapy for Parkinson's disease may have to rely on multiple drug interventions. © 2013 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Etienne C. Hirsch PhD</name><affiliations><json:string>Université Pierre et Marie Curie–Paris 06, Centre de Recherche de l'Institut du Cerveau et de la Moëlle Épinière, Hôpital de la Salpêtrière, Paris, France</json:string><json:string>Unité Mixte de Recherche U975, Institut National de la Santé et de la Recherche Médicale, Paris, France</json:string><json:string>Unité Mixte de Recherche 7225, Centre National de la Recherche Scientifique, Paris, France</json:string></affiliations></json:item><json:item><name>Peter Jenner PhD, DSc, FRPharmS</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, Institute of Pharmaceutical Sciences, School of Biomedical Sciences, King's College, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Serge Przedborski MD, PhD</name><affiliations><json:string>Department of Neurology, Department of Pathology and Cell Biology, and the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York</json:string><json:string>E-mail: sp30@columbia.edu</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Dopamine neuron</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>inflammation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurodegeneration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mitochndria</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>misfolded protein</value></json:item></subject><articleId><json:string>MDS25032</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>reviewArticle</json:string></originalGenre><abstract>Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. Currently, it is believed that the neurodegenerative process in Parkinson's disease is a combination of both cell‐autonomous and non‐cell‐autonomous mechanisms. Proposed cell‐autonomous mechanisms include alterations in mitochondrial bioenergetics, dysregulation of calcium homeostasis, and impaired turnover of mitochondria. As for the proposed non‐cell‐autonomous mechanisms, they involve prion‐like behavior of misfolded proteins and neuroinflammation. 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type="main" xml:lang="en">Pathogenesis of Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><availability><p>Copyright © 2013 Movement Disorder SocietyCopyright © 2013 Movement Disorders Society</p></availability><date>2013-02-06</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Pathogenesis of Parkinson's disease</title><author xml:id="author-1"><persName><forename type="first">Etienne C.</forename><surname>Hirsch</surname></persName><roleName type="degree">PhD</roleName><affiliation>Université Pierre et Marie Curie–Paris 06, Centre de Recherche de l'Institut du Cerveau et de la Moëlle Épinière, Hôpital de la Salpêtrière, Paris, France</affiliation><affiliation>Unité Mixte de Recherche U975, Institut National de la Santé et de la Recherche Médicale, Paris, France</affiliation><affiliation>Unité Mixte de Recherche 7225, Centre National de la Recherche Scientifique, Paris, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Peter</forename><surname>Jenner</surname></persName><roleName type="degree">PhD, DSc, FRPharmS</roleName><affiliation>Neurodegenerative Diseases Research Centre, Institute of Pharmaceutical Sciences, School of Biomedical Sciences, King's College, London, United Kingdom</affiliation></author><author xml:id="author-3"><persName><forename type="first">Serge</forename><surname>Przedborski</surname></persName><roleName type="degree">MD, PhD</roleName><email>sp30@columbia.edu</email><affiliation>Department of Neurology, Department of Pathology and Cell Biology, and the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov Disord</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><date type="published" when="2013-01"></date><biblScope unit="volume">28</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="24">24</biblScope><biblScope unit="page" to="30">30</biblScope></imprint></monogr><idno type="istex">169622838E7D6D3DB3B55A5455A3D2869BCB4F91</idno><idno type="DOI">10.1002/mds.25032</idno><idno type="ArticleID">MDS25032</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2013-02-06</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. 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<email>sp30@columbia.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS25032.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Pathogenesis of Parkinson's disease</title><title type="short">Pathogenesis of Parkinson's Disease</title></titleGroup><creators><creator affiliationRef="#mds25032-aff-0001 #mds25032-aff-0002 #mds25032-aff-0003" creatorRole="author" xml:id="mds25032-cr-0001"><personName><givenNames>Etienne C.</givenNames><familyName>Hirsch</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25032-aff-0004" creatorRole="author" xml:id="mds25032-cr-0002"><personName><givenNames>Peter</givenNames><familyName>Jenner</familyName><degrees>PhD, DSc, FRPharmS</degrees></personName></creator><creator affiliationRef="#mds25032-aff-0005" corresponding="yes" creatorRole="author" xml:id="mds25032-cr-0003"><personName><givenNames>Serge</givenNames><familyName>Przedborski</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation type="organization" xml:id="mds25032-aff-0001" countryCode="FR"><orgDiv>Université Pierre et Marie Curie–Paris 06, Centre de Recherche de l'Institut du Cerveau et de la Moëlle Épinière</orgDiv><orgName>Hôpital de la Salpêtrière</orgName><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25032-aff-0002" countryCode="FR"><orgName>Institut National de la Santé et de la Recherche Médicale</orgName><orgDiv>Unité Mixte de Recherche U975</orgDiv><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25032-aff-0003" countryCode="FR"><orgName>Centre National de la Recherche Scientifique</orgName><orgDiv>Unité Mixte de Recherche 7225</orgDiv><address><city>Paris</city><country>France</country></address></affiliation><affiliation type="organization" xml:id="mds25032-aff-0004" countryCode="GB"><orgDiv>Neurodegenerative Diseases Research Centre</orgDiv><orgDiv>Institute of Pharmaceutical Sciences</orgDiv><orgDiv>School of Biomedical Sciences</orgDiv><orgName>King's College</orgName><address><city>London</city><country>United Kingdom</country></address></affiliation><affiliation type="organization" xml:id="mds25032-aff-0005" countryCode="US"><orgDiv>Department of Neurology</orgDiv><orgDiv>Department of Pathology and Cell Biology, and the Center for Motor Neuron Biology and Disease</orgDiv><orgName>Columbia University</orgName><address><city>New York</city><countryPart>New York</countryPart></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="mds25032-kwd-0001">Dopamine neuron</keyword><keyword xml:id="mds25032-kwd-0002">inflammation</keyword><keyword xml:id="mds25032-kwd-0003">neurodegeneration</keyword><keyword xml:id="mds25032-kwd-0004">mitochndria</keyword><keyword xml:id="mds25032-kwd-0005">misfolded protein</keyword></keywordGroup><abstractGroup><abstract type="main"><p>Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. Currently, it is believed that the neurodegenerative process in Parkinson's disease is a combination of both cell‐autonomous and non‐cell‐autonomous mechanisms. Proposed cell‐autonomous mechanisms include alterations in mitochondrial bioenergetics, dysregulation of calcium homeostasis, and impaired turnover of mitochondria. As for the proposed non‐cell‐autonomous mechanisms, they involve prion‐like behavior of misfolded proteins and neuroinflammation. This suggests that cell death in Parkinson's disease is caused by a multifactorial cascade of pathogenic events and argues that effective neuroprotective therapy for Parkinson's disease may have to rely on multiple drug interventions. © 2013 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="mds25032-note-0001"><p><b>Relevant conflicts of interest/financial disclosures:</b> The authors are supported by grants from the National Institutes of Health (NS042269, NS064191, NS38370, NS070276, and NS072182 to S.P.), the U.S. Department of Defense (W81XWH‐08‐1‐0522, W81XWH‐08‐1‐0465, and W81XWH‐09‐1‐0245 to S.P.), the Parkinson Disease Foundation, the Thomas Hartman Foundation For Parkinson's Research, Project A.L.S, the Wings‐over‐Wall Street/Muscular Dystrophy Association. INSERM, CNRS, Université Pierre et Marie Curie, Cure Parkinson Foundation, Rosetrees Trust, Parkinson UK, and National Parkinson Foundation, Centre national de la recherche scientifique, Institut national de la santé et de la recherche médicale.</p></note><note xml:id="mds25032-note-0002"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Pathogenesis of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Pathogenesis of Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Pathogenesis of Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Etienne C.</namePart><namePart type="family">Hirsch</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Université Pierre et Marie Curie–Paris 06, Centre de Recherche de l'Institut du Cerveau et de la Moëlle Épinière, Hôpital de la Salpêtrière, Paris, France</affiliation><affiliation>Unité Mixte de Recherche U975, Institut National de la Santé et de la Recherche Médicale, Paris, France</affiliation><affiliation>Unité Mixte de Recherche 7225, Centre National de la Recherche Scientifique, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Jenner</namePart><namePart type="termsOfAddress">PhD, DSc, FRPharmS</namePart><affiliation>Neurodegenerative Diseases Research Centre, Institute of Pharmaceutical Sciences, School of Biomedical Sciences, King's College, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Serge</namePart><namePart type="family">Przedborski</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Department of Pathology and Cell Biology, and the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York</affiliation><affiliation>E-mail: sp30@columbia.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2013-01</dateIssued><dateCreated encoding="w3cdtf">2013-02-06</dateCreated><dateCaptured encoding="w3cdtf">2012-01-09</dateCaptured><dateValid encoding="w3cdtf">2012-04-08</dateValid><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. Currently, it is believed that the neurodegenerative process in Parkinson's disease is a combination of both cell‐autonomous and non‐cell‐autonomous mechanisms. Proposed cell‐autonomous mechanisms include alterations in mitochondrial bioenergetics, dysregulation of calcium homeostasis, and impaired turnover of mitochondria. As for the proposed non‐cell‐autonomous mechanisms, they involve prion‐like behavior of misfolded proteins and neuroinflammation. This suggests that cell death in Parkinson's disease is caused by a multifactorial cascade of pathogenic events and argues that effective neuroprotective therapy for Parkinson's disease may have to rely on multiple drug interventions. © 2013 Movement Disorder Society</abstract><subject><genre>keywords</genre><topic>Dopamine neuron</topic><topic>inflammation</topic><topic>neurodegeneration</topic><topic>mitochndria</topic><topic>misfolded protein</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov Disord</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Review</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>2013</date><detail type="title"><title>The Vatican Conference on Neuroprotection in Parkinson's Disease</title></detail><detail type="volume"><caption>vol.</caption><number>28</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>24</start><end>30</end><total>7</total></extent></part></relatedItem><identifier type="istex">169622838E7D6D3DB3B55A5455A3D2869BCB4F91</identifier><identifier type="DOI">10.1002/mds.25032</identifier><identifier type="ArticleID">MDS25032</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2013 Movement Disorder SocietyCopyright © 2013 Movement Disorders Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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