Mitochondrial therapies for Parkinson's disease
Identifieur interne : 001150 ( Main/Corpus ); précédent : 001149; suivant : 001151Mitochondrial therapies for Parkinson's disease
Auteurs : Bobby Thomas ; M. Flint BealSource :
- Movement Disorders [ 0885-3185 ] ; 2010.
English descriptors
Abstract
Parkinson's disease (PD) is marked by widespread neurodegeneration in the brain in addition to a selective yet prominent and progressive loss of nigrostriatal dopaminergic neurons. Of the multiple theories suggested in the pathogenesis of PD, mitochondrial dysfunction takes a center stage in both sporadic and familial forms of illness. Deficits in mitochondrial functions due to impaired bioenergetics, aging associated increased generation of reactive oxygen species, damage to mitochondrial DNA, impaired calcium buffering, and alterations in mitochondrial morphology may contribute to improper functioning of the CNS leading to neurodegeneration. These mitochondrial alterations suggest that a potential target worth exploring for neuroprotective therapies are the ones that can preserve mitochondrial functions in PD. Here, we provide a recent update on potential drugs that are known to block mitochondrial dysfunctions in various experimental models and those that are currently under clinical trials for PD. We also review novel mitochondrial survival pathways that provide hope and promise for innovative neuroprotective therapies in the future that can be explored as possible therapeutic intervention for PD pathogenesis. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22781
Links to Exploration step
ISTEX:AAC0A505362843018C95F568E14B50A308B85969Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mitochondrial therapies for Parkinson's disease</title><author><name sortKey="Thomas, Bobby" sort="Thomas, Bobby" uniqKey="Thomas B" first="Bobby" last="Thomas">Bobby Thomas</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:AAC0A505362843018C95F568E14B50A308B85969</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1002/mds.22781</idno><idno type="url">https://api.istex.fr/document/AAC0A505362843018C95F568E14B50A308B85969/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001150</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Mitochondrial therapies for Parkinson's disease</title><author><name sortKey="Thomas, Bobby" sort="Thomas, Bobby" uniqKey="Thomas B" first="Bobby" last="Thomas">Bobby Thomas</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010">2010</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="page" from="S155">S155</biblScope><biblScope unit="page" to="S160">S160</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">AAC0A505362843018C95F568E14B50A308B85969</idno><idno type="DOI">10.1002/mds.22781</idno><idno type="ArticleID">MDS22781</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PGC‐1α</term><term>Parkinson's disease</term><term>coenzyme Q10</term><term>creatine</term><term>mitochondrial dysfunction</term><term>sirtuins</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is marked by widespread neurodegeneration in the brain in addition to a selective yet prominent and progressive loss of nigrostriatal dopaminergic neurons. Of the multiple theories suggested in the pathogenesis of PD, mitochondrial dysfunction takes a center stage in both sporadic and familial forms of illness. Deficits in mitochondrial functions due to impaired bioenergetics, aging associated increased generation of reactive oxygen species, damage to mitochondrial DNA, impaired calcium buffering, and alterations in mitochondrial morphology may contribute to improper functioning of the CNS leading to neurodegeneration. These mitochondrial alterations suggest that a potential target worth exploring for neuroprotective therapies are the ones that can preserve mitochondrial functions in PD. Here, we provide a recent update on potential drugs that are known to block mitochondrial dysfunctions in various experimental models and those that are currently under clinical trials for PD. We also review novel mitochondrial survival pathways that provide hope and promise for innovative neuroprotective therapies in the future that can be explored as possible therapeutic intervention for PD pathogenesis. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Bobby Thomas PhD</name><affiliations><json:string>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</json:string></affiliations></json:item><json:item><name>M. Flint Beal MD</name><affiliations><json:string>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mitochondrial dysfunction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>coenzyme Q10</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>creatine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PGC‐1α</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sirtuins</value></json:item></subject><articleId><json:string>MDS22781</json:string></articleId><language><json:string>eng</json:string></language><abstract>Parkinson's disease (PD) is marked by widespread neurodegeneration in the brain in addition to a selective yet prominent and progressive loss of nigrostriatal dopaminergic neurons. Of the multiple theories suggested in the pathogenesis of PD, mitochondrial dysfunction takes a center stage in both sporadic and familial forms of illness. Deficits in mitochondrial functions due to impaired bioenergetics, aging associated increased generation of reactive oxygen species, damage to mitochondrial DNA, impaired calcium buffering, and alterations in mitochondrial morphology may contribute to improper functioning of the CNS leading to neurodegeneration. These mitochondrial alterations suggest that a potential target worth exploring for neuroprotective therapies are the ones that can preserve mitochondrial functions in PD. Here, we provide a recent update on potential drugs that are known to block mitochondrial dysfunctions in various experimental models and those that are currently under clinical trials for PD. We also review novel mitochondrial survival pathways that provide hope and promise for innovative neuroprotective therapies in the future that can be explored as possible therapeutic intervention for PD pathogenesis. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>6.066</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1266</abstractCharCount><pdfWordCount>3954</pdfWordCount><pdfCharCount>27181</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>176</abstractWordCount></qualityIndicators><title>Mitochondrial therapies for Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>25</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>6</total><last>S160</last><first>S155</first></pages><issn><json:string>0885-3185</json:string></issn><issue>S1</issue><author><json:item><name>Fahn Stanley MD</name></json:item><json:item><name>Marder Karen MD</name></json:item><json:item><name>Côté Lucien MD</name></json:item><json:item><name>Reich Stephen G. MD</name></json:item></author><subject><json:item><value>Future Developments in Treatment of PD</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.22781</json:string></doi><id>AAC0A505362843018C95F568E14B50A308B85969</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/AAC0A505362843018C95F568E14B50A308B85969/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/AAC0A505362843018C95F568E14B50A308B85969/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/AAC0A505362843018C95F568E14B50A308B85969/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mitochondrial therapies for Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None reported.</note><note>National Institutes of Health</note><note>Michael J Fox Foundation for Parkinson's disease</note><note>Department of Defense</note><note>Parkinson's disease Foundation</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mitochondrial therapies for Parkinson's disease</title><author><persName><forename type="first">Bobby</forename><surname>Thomas</surname></persName><roleName type="degree">PhD</roleName><note type="correspondence"><p>Correspondence: Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A‐501, New York, New York 10065</p></note><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</affiliation></author><author><persName><forename type="first">M. Flint</forename><surname>Beal</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A‐501, New York, New York 10065</p></note><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</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>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010"></date><biblScope unit="volume">25</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="page" from="S155">S155</biblScope><biblScope unit="page" to="S160">S160</biblScope></imprint></monogr><idno type="istex">AAC0A505362843018C95F568E14B50A308B85969</idno><idno type="DOI">10.1002/mds.22781</idno><idno type="ArticleID">MDS22781</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Parkinson's disease (PD) is marked by widespread neurodegeneration in the brain in addition to a selective yet prominent and progressive loss of nigrostriatal dopaminergic neurons. Of the multiple theories suggested in the pathogenesis of PD, mitochondrial dysfunction takes a center stage in both sporadic and familial forms of illness. Deficits in mitochondrial functions due to impaired bioenergetics, aging associated increased generation of reactive oxygen species, damage to mitochondrial DNA, impaired calcium buffering, and alterations in mitochondrial morphology may contribute to improper functioning of the CNS leading to neurodegeneration. These mitochondrial alterations suggest that a potential target worth exploring for neuroprotective therapies are the ones that can preserve mitochondrial functions in PD. Here, we provide a recent update on potential drugs that are known to block mitochondrial dysfunctions in various experimental models and those that are currently under clinical trials for PD. We also review novel mitochondrial survival pathways that provide hope and promise for innovative neuroprotective therapies in the future that can be explored as possible therapeutic intervention for PD pathogenesis. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>mitochondrial dysfunction</term></item><item><term>coenzyme Q10</term></item><item><term>creatine</term></item><item><term>PGC‐1α</term></item><item><term>sirtuins</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Future Developments in Treatment of PD</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-12-19">Received</change><change when="2009-08-21">Registration</change><change when="2010">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/AAC0A505362843018C95F568E14B50A308B85969/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="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="5"><doi origin="wiley" registered="yes">10.1002/mds.v25.1s</doi><titleGroup><title type="specialIssueTitle">Frontiers of Science and Clinical Advances in Quality of Life in Parkinson's Disease</title></titleGroup><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">S1</numbering></numberingGroup><creators><creator xml:id="sped1" creatorRole="sponsoringEditor"><personName><givenNames>Fahn</givenNames><familyName>Stanley</familyName><degrees>MD</degrees></personName></creator><creator xml:id="sped2" creatorRole="sponsoringEditor"><personName><givenNames>Marder</givenNames><familyName>Karen</familyName><degrees>MD</degrees></personName></creator><creator xml:id="sped3" creatorRole="sponsoringEditor"><personName><givenNames>Côté</givenNames><familyName>Lucien</familyName><degrees>MD</degrees></personName></creator><creator xml:id="sped4" creatorRole="sponsoringEditor"><personName><givenNames>Reich</givenNames><familyName>Stephen G.</familyName><degrees>MD</degrees></personName></creator></creators><coverDate startDate="2010">2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="29" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.22781</doi><idGroup><id type="unit" value="MDS22781"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Future Developments in Treatment of PD</title><title type="tocHeading1">Future Developments in Treatment of PD</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2007-12-19"></event><event type="manuscriptAccepted" date="2009-08-21"></event><event type="firstOnline" date="2010-02-25"></event><event type="publishedOnlineFinalForm" date="2010-02-25"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4 mode:FullText" date="2010-12-14"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">S155</numbering><numbering type="pageLast">S160</numbering></numberingGroup><correspondenceTo>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A‐501, New York, New York 10065</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS22781.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="70"></count><count type="wordTotal" number="3877"></count></countGroup><titleGroup><title type="main" xml:lang="en">Mitochondrial therapies for Parkinson's disease<link href="#fn1"></link></title><title type="short" xml:lang="en">Mitochondria and Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Bobby</givenNames><familyName>Thomas</familyName><degrees>PhD</degrees></personName><contactDetails><email>bot2003@med.cornell.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>M. Flint</givenNames><familyName>Beal</familyName><degrees>MD</degrees></personName><contactDetails><email>fbeal@med.cornell.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">mitochondrial dysfunction</keyword><keyword xml:id="kwd3">coenzyme Q10</keyword><keyword xml:id="kwd4">creatine</keyword><keyword xml:id="kwd5">PGC‐1α</keyword><keyword xml:id="kwd6">sirtuins</keyword></keywordGroup><fundingInfo><fundingAgency>National Institutes of Health</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Michael J Fox Foundation for Parkinson's disease</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Department of Defense</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Parkinson's disease Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson's disease (PD) is marked by widespread neurodegeneration in the brain in addition to a selective yet prominent and progressive loss of nigrostriatal dopaminergic neurons. Of the multiple theories suggested in the pathogenesis of PD, mitochondrial dysfunction takes a center stage in both sporadic and familial forms of illness. Deficits in mitochondrial functions due to impaired bioenergetics, aging associated increased generation of reactive oxygen species, damage to mitochondrial DNA, impaired calcium buffering, and alterations in mitochondrial morphology may contribute to improper functioning of the CNS leading to neurodegeneration. These mitochondrial alterations suggest that a potential target worth exploring for neuroprotective therapies are the ones that can preserve mitochondrial functions in PD. Here, we provide a recent update on potential drugs that are known to block mitochondrial dysfunctions in various experimental models and those that are currently under clinical trials for PD. We also review novel mitochondrial survival pathways that provide hope and promise for innovative neuroprotective therapies in the future that can be explored as possible therapeutic intervention for PD pathogenesis. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mitochondrial therapies for Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Mitochondria and Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mitochondrial therapies for Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Bobby</namePart><namePart type="family">Thomas</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</affiliation><description>Correspondence: Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A‐501, New York, New York 10065</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. Flint</namePart><namePart type="family">Beal</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</affiliation><description>Correspondence: Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A‐501, New York, New York 10065</description><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">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010</dateIssued><dateCaptured encoding="w3cdtf">2007-12-19</dateCaptured><dateValid encoding="w3cdtf">2009-08-21</dateValid><copyrightDate encoding="w3cdtf">2010</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="references">70</extent><extent unit="words">3877</extent></physicalDescription><abstract lang="en">Parkinson's disease (PD) is marked by widespread neurodegeneration in the brain in addition to a selective yet prominent and progressive loss of nigrostriatal dopaminergic neurons. Of the multiple theories suggested in the pathogenesis of PD, mitochondrial dysfunction takes a center stage in both sporadic and familial forms of illness. Deficits in mitochondrial functions due to impaired bioenergetics, aging associated increased generation of reactive oxygen species, damage to mitochondrial DNA, impaired calcium buffering, and alterations in mitochondrial morphology may contribute to improper functioning of the CNS leading to neurodegeneration. These mitochondrial alterations suggest that a potential target worth exploring for neuroprotective therapies are the ones that can preserve mitochondrial functions in PD. Here, we provide a recent update on potential drugs that are known to block mitochondrial dysfunctions in various experimental models and those that are currently under clinical trials for PD. We also review novel mitochondrial survival pathways that provide hope and promise for innovative neuroprotective therapies in the future that can be explored as possible therapeutic intervention for PD pathogenesis. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">National Institutes of Health</note><note type="funding">Michael J Fox Foundation for Parkinson's disease</note><note type="funding">Department of Defense</note><note type="funding">Parkinson's disease Foundation</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>mitochondrial dysfunction</topic><topic>coenzyme Q10</topic><topic>creatine</topic><topic>PGC‐1α</topic><topic>sirtuins</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><name type="personal"><namePart type="given">Fahn</namePart><namePart type="family">Stanley</namePart><namePart type="termsOfAddress">MD</namePart></name><name type="personal"><namePart type="given">Marder</namePart><namePart type="family">Karen</namePart><namePart type="termsOfAddress">MD</namePart></name><name type="personal"><namePart type="given">Côté</namePart><namePart type="family">Lucien</namePart><namePart type="termsOfAddress">MD</namePart></name><name type="personal"><namePart type="given">Reich</namePart><namePart type="family">Stephen G.</namePart><namePart type="termsOfAddress">MD</namePart></name><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Future Developments in Treatment of PD</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>2010</date><detail type="title"><title>Frontiers of Science and Clinical Advances in Quality of Life in Parkinson's Disease</title></detail><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>S1</number></detail><extent unit="pages"><start>S155</start><end>S160</end><total>6</total></extent></part></relatedItem><identifier type="istex">AAC0A505362843018C95F568E14B50A308B85969</identifier><identifier type="DOI">10.1002/mds.22781</identifier><identifier type="ArticleID">MDS22781</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</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)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001150 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 001150 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:AAC0A505362843018C95F568E14B50A308B85969
|texte= Mitochondrial therapies for Parkinson's disease
}}
| This area was generated with Dilib version V0.6.23. |  |