Mitochondrial respiratory chain function in multiple system atrophy
Identifieur interne : 002B44 ( Istex/Corpus ); précédent : 002B43; suivant : 002B45Mitochondrial respiratory chain function in multiple system atrophy
Auteurs : M. Gu ; M. T. Gash ; J. M. Cooper ; G. K. Wenning ; S. E. Daniel ; N. P. Quinn ; C. D. Marsden ; SchapiraSource :
- Movement Disorders [ 0885-3185 ] ; 1997-05.
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- KwdEn :
Abstract
Multiple system atrophy (MSA) is a clinicopathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5–10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L‐DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L‐DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.
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DOI: 10.1002/mds.870120323
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ISTEX:8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67FLe document en format XML
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Marsden</name><affiliation><mods:affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</mods:affiliation></affiliation></author><author><name sortKey="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name><affiliation><mods:affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</mods:affiliation></affiliation><affiliation><mods:affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1997-05">1997-05</date><biblScope unit="vol">12</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="418">418</biblScope><biblScope unit="page" to="422">422</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F</idno><idno type="DOI">10.1002/mds.870120323</idno><idno type="ArticleID">MDS870120323</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>L‐DOPA</term><term>Mitochondria</term><term>Multiple system atrophy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Multiple system atrophy (MSA) is a clinicopathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5–10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L‐DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L‐DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>M. Gu</name><affiliations><json:string>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</json:string></affiliations></json:item><json:item><name>M. T. Gash</name><affiliations><json:string>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</json:string></affiliations></json:item><json:item><name>J. M. Cooper</name><affiliations><json:string>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</json:string></affiliations></json:item><json:item><name>G. K. Wenning</name><affiliations><json:string>University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>S. E. Daniel</name><affiliations><json:string>Parkinson's Disease Society Brain Bank, London, England</json:string></affiliations></json:item><json:item><name>N. P. Quinn</name><affiliations><json:string>University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>C. D. Marsden</name><affiliations><json:string>University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item><json:item><name>Prof. Schapira</name><affiliations><json:string>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</json:string><json:string>University Department of Clinical Neurology, Institute of Neurology, London, England</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Multiple system atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Mitochondria</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>L‐DOPA</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Multiple system atrophy (MSA) is a clinicopathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5–10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L‐DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L‐DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.</abstract><qualityIndicators><score>4.646</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 827.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1145</abstractCharCount><pdfWordCount>2498</pdfWordCount><pdfCharCount>15822</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>179</abstractWordCount></qualityIndicators><title>Mitochondrial respiratory chain function in multiple system atrophy</title><genre><json:string>Serial article</json:string></genre><host><volume>12</volume><pages><total>5</total><last>422</last><first>418</first></pages><issn><json:string>0885-3185</json:string></issn><issue>3</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1002/mds.870120323</json:string></doi><id>8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mitochondrial respiratory chain function in multiple system atrophy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1997</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mitochondrial respiratory chain function in multiple system atrophy</title><author><persName><forename type="first">M.</forename><surname>Gu</surname></persName><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation></author><author><persName><forename type="first">M. T.</forename><surname>Gash</surname></persName><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation></author><author><persName><forename type="first">J. M.</forename><surname>Cooper</surname></persName><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation></author><author><persName><forename type="first">G. K.</forename><surname>Wenning</surname></persName><affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation></author><author><persName><forename type="first">S. E.</forename><surname>Daniel</surname></persName><affiliation>Parkinson's Disease Society Brain Bank, London, England</affiliation></author><author><persName><forename type="first">N. 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D.</forename><surname>Marsden</surname></persName><affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation></author><author><persName><surname>Schapira</surname><roleName type="degree">Prof.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, Rowland Hill Street, London NW3 2PF, England</p></note><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation><affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1997-05"></date><biblScope unit="vol">12</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="418">418</biblScope><biblScope unit="page" to="422">422</biblScope></imprint></monogr><idno type="istex">8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F</idno><idno type="DOI">10.1002/mds.870120323</idno><idno type="ArticleID">MDS870120323</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Multiple system atrophy (MSA) is a clinicopathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5–10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L‐DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L‐DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Multiple system atrophy</term></item><item><term>Mitochondria</term></item><item><term>L‐DOPA</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-01-25">Received</change><change when="1996-08-02">Registration</change><change when="1997-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F/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>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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T.</givenNames><familyName>Gash</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>J. M.</givenNames><familyName>Cooper</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>G. K.</givenNames><familyName>Wenning</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>S. E.</givenNames><familyName>Daniel</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>N. P.</givenNames><familyName>Quinn</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>C. 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V.</givenNames><familyName>Schapira</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Parkinson's Disease Society Brain Bank, London, England</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Multiple system atrophy</keyword><keyword xml:id="kwd2">Mitochondria</keyword><keyword xml:id="kwd3">L‐DOPA</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Multiple system atrophy (MSA) is a clinicopathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5–10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L‐DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L‐DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Mitochondrial respiratory chain function in multiple system atrophy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>MITOCHONDRIAL RESPIRATORY CHAIN FUNCTION IN MSA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mitochondrial respiratory chain function in multiple system atrophy</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Gu</namePart><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. T.</namePart><namePart type="family">Gash</namePart><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. M.</namePart><namePart type="family">Cooper</namePart><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G. K.</namePart><namePart type="family">Wenning</namePart><affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. E.</namePart><namePart type="family">Daniel</namePart><affiliation>Parkinson's Disease Society Brain Bank, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N. P.</namePart><namePart type="family">Quinn</namePart><affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. D.</namePart><namePart type="family">Marsden</namePart><affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Prof.</namePart><namePart type="family">Schapira</namePart><affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England</affiliation><affiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</affiliation><description>Correspondence: Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, Rowland Hill Street, London NW3 2PF, England</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">1997-05</dateIssued><dateCaptured encoding="w3cdtf">1996-01-25</dateCaptured><dateValid encoding="w3cdtf">1996-08-02</dateValid><copyrightDate encoding="w3cdtf">1997</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">1</extent><extent unit="tables">4</extent><extent unit="references">17</extent></physicalDescription><abstract lang="en">Multiple system atrophy (MSA) is a clinicopathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5–10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L‐DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L‐DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.</abstract><subject lang="en"><genre>Keywords</genre><topic>Multiple system atrophy</topic><topic>Mitochondria</topic><topic>L‐DOPA</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>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>1997</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>418</start><end>422</end><total>5</total></extent></part></relatedItem><identifier type="istex">8020DF8A1F61EB22FAB621F07CD7FEF0E5DED67F</identifier><identifier type="DOI">10.1002/mds.870120323</identifier><identifier type="ArticleID">MDS870120323</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 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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