Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration
Identifieur interne : 002404 ( Main/Corpus ); précédent : 002403; suivant : 002405Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration
Auteurs : Yuen-Sum Lau ; Gaurav Patki ; Kaberi Das-Panja ; Wei-Dong Le ; S. Omar AhmadSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2011-04.
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Abstract
The protective impact of exercise on neurodegenerative processes has not been confirmed, and the mechanisms underlying the benefit of exercise have not been determined in human Parkinson’s disease or in chronic animal disease models. This research examined the long‐term neurological, behavioral, and mechanistic consequences of endurance exercise in experimental chronic parkinsonism. We used a chronic 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐induced mouse model of Parkinson’s disease with moderate neurodegeneration and examined the effects of treadmill exercise on movement and balance coordination, changes in dopamine neuron biomarkers, mitochondrial functions, and neurotrophic factor activities in the nigrostriatal system. The exercise results were compared with those of the control and sedentary chronic parkinsonian animals. After 18 weeks of exercise training in the chronic parkinsonian mice, we observed a significant deterrence in the loss of neuronal dopamine‐producing cells and other functional indicators. The impaired movement and balance incoordination in the chronic parkinsonian mice were also markedly reduced following exercise. Mechanistic investigations revealed that the neuronal and behavioral recovery produced by exercise in the chronic parkinsonian mice was associated with an improved mitochondrial function and an increase in the brain region‐specific levels of brain‐derived and glial cell line‐derived neurotrophic factors. Our findings indicate that exercise not only produces neuronal and mitochondrial protection, it also boosts nigrostriatal neurotrophic factor levels in the chronic parkinsonian mice with moderate neurodegeneration. Therefore, modifying lifestyle with increased exercise activity would be a non‐pharmacological neuroprotective approach for averting neurodegenerative processes, as demonstrated in experimental chronic parkinsonism.
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DOI: 10.1111/j.1460-9568.2011.07626.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration</title><author><name sortKey="Lau, Yuen Um" sort="Lau, Yuen Um" uniqKey="Lau Y" first="Yuen-Sum" last="Lau">Yuen-Sum Lau</name><affiliation><mods:affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</mods:affiliation></affiliation></author><author><name sortKey="Patki, Gaurav" sort="Patki, Gaurav" uniqKey="Patki G" first="Gaurav" last="Patki">Gaurav Patki</name><affiliation><mods:affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</mods:affiliation></affiliation></author><author><name sortKey="Das Anja, Kaberi" sort="Das Anja, Kaberi" uniqKey="Das Anja K" first="Kaberi" last="Das-Panja">Kaberi Das-Panja</name><affiliation><mods:affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</mods:affiliation></affiliation></author><author><name sortKey="Le, Wei Ong" sort="Le, Wei Ong" uniqKey="Le W" first="Wei-Dong" last="Le">Wei-Dong Le</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, TX, USA</mods:affiliation></affiliation></author><author><name sortKey="Ahmad, S Omar" sort="Ahmad, S Omar" uniqKey="Ahmad S" first="S. 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Omar Ahmad</name><affiliation><mods:affiliation>Department of Occupational Therapy Education, Kansas University Medical Center, Kansas City, KS, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:963389C1F0EAB819253624453753C00A4F447E29</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1111/j.1460-9568.2011.07626.x</idno><idno type="url">https://api.istex.fr/document/963389C1F0EAB819253624453753C00A4F447E29/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002404</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration</title><author><name sortKey="Lau, Yuen Um" sort="Lau, Yuen Um" uniqKey="Lau Y" first="Yuen-Sum" last="Lau">Yuen-Sum Lau</name><affiliation><mods:affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</mods:affiliation></affiliation></author><author><name sortKey="Patki, Gaurav" sort="Patki, Gaurav" uniqKey="Patki G" first="Gaurav" last="Patki">Gaurav Patki</name><affiliation><mods:affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</mods:affiliation></affiliation></author><author><name sortKey="Das Anja, Kaberi" sort="Das Anja, Kaberi" uniqKey="Das Anja K" first="Kaberi" last="Das-Panja">Kaberi Das-Panja</name><affiliation><mods:affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</mods:affiliation></affiliation></author><author><name sortKey="Le, Wei Ong" sort="Le, Wei Ong" uniqKey="Le W" first="Wei-Dong" last="Le">Wei-Dong Le</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, TX, USA</mods:affiliation></affiliation></author><author><name sortKey="Ahmad, S Omar" sort="Ahmad, S Omar" uniqKey="Ahmad S" first="S. 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Omar Ahmad</name><affiliation><mods:affiliation>Department of Occupational Therapy Education, Kansas University Medical Center, Kansas City, KS, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neuroscience</title><idno type="ISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-04">2011-04</date><biblScope unit="volume">33</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1264">1264</biblScope><biblScope unit="page" to="1274">1274</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">963389C1F0EAB819253624453753C00A4F447E29</idno><idno type="DOI">10.1111/j.1460-9568.2011.07626.x</idno><idno type="ArticleID">EJN7626</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine parkinsonism</term><term>endurance exercise</term><term>mitochondrial dysfunction</term><term>neuroprotection</term><term>neurotrophic factor</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The protective impact of exercise on neurodegenerative processes has not been confirmed, and the mechanisms underlying the benefit of exercise have not been determined in human Parkinson’s disease or in chronic animal disease models. This research examined the long‐term neurological, behavioral, and mechanistic consequences of endurance exercise in experimental chronic parkinsonism. We used a chronic 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐induced mouse model of Parkinson’s disease with moderate neurodegeneration and examined the effects of treadmill exercise on movement and balance coordination, changes in dopamine neuron biomarkers, mitochondrial functions, and neurotrophic factor activities in the nigrostriatal system. The exercise results were compared with those of the control and sedentary chronic parkinsonian animals. After 18 weeks of exercise training in the chronic parkinsonian mice, we observed a significant deterrence in the loss of neuronal dopamine‐producing cells and other functional indicators. The impaired movement and balance incoordination in the chronic parkinsonian mice were also markedly reduced following exercise. Mechanistic investigations revealed that the neuronal and behavioral recovery produced by exercise in the chronic parkinsonian mice was associated with an improved mitochondrial function and an increase in the brain region‐specific levels of brain‐derived and glial cell line‐derived neurotrophic factors. Our findings indicate that exercise not only produces neuronal and mitochondrial protection, it also boosts nigrostriatal neurotrophic factor levels in the chronic parkinsonian mice with moderate neurodegeneration. Therefore, modifying lifestyle with increased exercise activity would be a non‐pharmacological neuroprotective approach for averting neurodegenerative processes, as demonstrated in experimental chronic parkinsonism.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Yuen‐Sum Lau</name><affiliations><json:string>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</json:string></affiliations></json:item><json:item><name>Gaurav Patki</name><affiliations><json:string>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</json:string></affiliations></json:item><json:item><name>Kaberi Das‐Panja</name><affiliations><json:string>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</json:string></affiliations></json:item><json:item><name>Wei‐Dong Le</name><affiliations><json:string>Department of Neurology, Baylor College of Medicine, Houston, TX, USA</json:string></affiliations></json:item><json:item><name>S. Omar Ahmad</name><affiliations><json:string>Department of Occupational Therapy Education, Kansas University Medical Center, Kansas City, KS, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>endurance exercise</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>neuroprotection</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurotrophic factor</value></json:item></subject><articleId><json:string>EJN7626</json:string></articleId><language><json:string>eng</json:string></language><abstract>The protective impact of exercise on neurodegenerative processes has not been confirmed, and the mechanisms underlying the benefit of exercise have not been determined in human Parkinson’s disease or in chronic animal disease models. 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Mechanistic investigations revealed that the neuronal and behavioral recovery produced by exercise in the chronic parkinsonian mice was associated with an improved mitochondrial function and an increase in the brain region‐specific levels of brain‐derived and glial cell line‐derived neurotrophic factors. Our findings indicate that exercise not only produces neuronal and mitochondrial protection, it also boosts nigrostriatal neurotrophic factor levels in the chronic parkinsonian mice with moderate neurodegeneration. 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Omar</forename><surname>Ahmad</surname></persName><affiliation>Department of Occupational Therapy Education, Kansas University Medical Center, Kansas City, KS, USA</affiliation></author></analytic><monogr><title level="j">European Journal of Neuroscience</title><idno type="pISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><idno type="DOI">10.1111/(ISSN)1460-9568</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-04"></date><biblScope unit="volume">33</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1264">1264</biblScope><biblScope unit="page" to="1274">1274</biblScope></imprint></monogr><idno type="istex">963389C1F0EAB819253624453753C00A4F447E29</idno><idno type="DOI">10.1111/j.1460-9568.2011.07626.x</idno><idno type="ArticleID">EJN7626</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The protective impact of exercise on neurodegenerative processes has not been confirmed, and the mechanisms underlying the benefit of exercise have not been determined in human Parkinson’s disease or in chronic animal disease models. This research examined the long‐term neurological, behavioral, and mechanistic consequences of endurance exercise in experimental chronic parkinsonism. We used a chronic 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐induced mouse model of Parkinson’s disease with moderate neurodegeneration and examined the effects of treadmill exercise on movement and balance coordination, changes in dopamine neuron biomarkers, mitochondrial functions, and neurotrophic factor activities in the nigrostriatal system. The exercise results were compared with those of the control and sedentary chronic parkinsonian animals. After 18 weeks of exercise training in the chronic parkinsonian mice, we observed a significant deterrence in the loss of neuronal dopamine‐producing cells and other functional indicators. The impaired movement and balance incoordination in the chronic parkinsonian mice were also markedly reduced following exercise. Mechanistic investigations revealed that the neuronal and behavioral recovery produced by exercise in the chronic parkinsonian mice was associated with an improved mitochondrial function and an increase in the brain region‐specific levels of brain‐derived and glial cell line‐derived neurotrophic factors. Our findings indicate that exercise not only produces neuronal and mitochondrial protection, it also boosts nigrostriatal neurotrophic factor levels in the chronic parkinsonian mice with moderate neurodegeneration. Therefore, modifying lifestyle with increased exercise activity would be a non‐pharmacological neuroprotective approach for averting neurodegenerative processes, as demonstrated in experimental chronic parkinsonism.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine parkinsonism</term></item><item><term>endurance exercise</term></item><item><term>mitochondrial dysfunction</term></item><item><term>neuroprotection</term></item><item><term>neurotrophic factor</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>NEUROSYSTEMS</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-04">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/963389C1F0EAB819253624453753C00A4F447E29/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="04107"><doi origin="wiley">10.1111/ejn.2011.33.issue-7</doi><numberingGroup><numbering type="journalVolume" number="33">33</numbering><numbering type="journalIssue" number="7">7</numbering></numberingGroup><coverDate startDate="2011-04">April 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="10" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2011.07626.x</doi><idGroup><id type="unit" value="EJN7626"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="tocHeading1">NEUROSYSTEMS</title><title type="articleCategory">NEUROSYSTEMS</title></titleGroup><copyright>© 2011 The Authors. European Journal of Neuroscience © 2011 Federation of European Neuroscience Societies and Blackwell Publishing Ltd</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.4.8 mode:FullText" date="2011-04-03"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-03-07"></event><event type="firstOnline" date="2011-03-07"></event><event type="publishedOnlineFinalForm" date="2011-04-03"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-17"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1264">1264</numbering><numbering type="pageLast" number="1274">1274</numbering></numberingGroup><correspondenceTo>Y.‐S. Lau, as above.
E‐mail: <email>ylau2@uh.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN7626.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 30 September 2010, accepted 6 January 2011</unparsedEditorialHistory><countGroup><count type="figureTotal" number="7"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration</title><title type="shortAuthors">Y.‐S. Lau <i>et al.</i></title><title type="short">Exercise neuroprotection in chronic parkinsonism</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Yuen‐Sum</givenNames><familyName>Lau</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Gaurav</givenNames><familyName>Patki</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Kaberi</givenNames><familyName>Das‐Panja</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>Wei‐Dong</givenNames><familyName>Le</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a3"><personName><givenNames>S. Omar</givenNames><familyName>Ahmad</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Department of Neurology, Baylor College of Medicine, Houston, TX, USA</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="US"><unparsedAffiliation>Department of Occupational Therapy Education, Kansas University Medical Center, Kansas City, KS, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine parkinsonism</keyword><keyword xml:id="k2">endurance exercise</keyword><keyword xml:id="k3">mitochondrial dysfunction</keyword><keyword xml:id="k4">neuroprotection</keyword><keyword xml:id="k5">neurotrophic factor</keyword></keywordGroup><supportingInformation><p>Figure S1. Nigrostriatal effects of 10 weeks of exercise in chronic MPD.</p><p>Table S1. Summary and comparison of exercise studies in rodent models of PD.</p><p>As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer‐reviewed and may be re‐organized for online delivery, but are not copy‐edited or typeset by Wiley‐Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors.</p><supportingInfoItem><mediaResource alt="supporting info item" href="urn-x:wiley:0953816X:media:ejn7626:EJN_7626_sm_figureS1-legend"></mediaResource><caption>Supporting info item</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting info item" href="urn-x:wiley:0953816X:media:ejn7626:EJN_7626_sm_figureS1"></mediaResource><caption>Supporting info item</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting info item" href="urn-x:wiley:0953816X:media:ejn7626:EJN_7626_sm_tableS1"></mediaResource><caption>Supporting info item</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The protective impact of exercise on neurodegenerative processes has not been confirmed, and the mechanisms underlying the benefit of exercise have not been determined in human Parkinson’s disease or in chronic animal disease models. This research examined the long‐term neurological, behavioral, and mechanistic consequences of endurance exercise in experimental chronic parkinsonism. We used a chronic 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐induced mouse model of Parkinson’s disease with moderate neurodegeneration and examined the effects of treadmill exercise on movement and balance coordination, changes in dopamine neuron biomarkers, mitochondrial functions, and neurotrophic factor activities in the nigrostriatal system. The exercise results were compared with those of the control and sedentary chronic parkinsonian animals. After 18 weeks of exercise training in the chronic parkinsonian mice, we observed a significant deterrence in the loss of neuronal dopamine‐producing cells and other functional indicators. The impaired movement and balance incoordination in the chronic parkinsonian mice were also markedly reduced following exercise. Mechanistic investigations revealed that the neuronal and behavioral recovery produced by exercise in the chronic parkinsonian mice was associated with an improved mitochondrial function and an increase in the brain region‐specific levels of brain‐derived and glial cell line‐derived neurotrophic factors. Our findings indicate that exercise not only produces neuronal and mitochondrial protection, it also boosts nigrostriatal neurotrophic factor levels in the chronic parkinsonian mice with moderate neurodegeneration. Therefore, modifying lifestyle with increased exercise activity would be a non‐pharmacological neuroprotective approach for averting neurodegenerative processes, as demonstrated in experimental chronic parkinsonism.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration</title></titleInfo><titleInfo type="abbreviated"><title>Exercise neuroprotection in chronic parkinsonism</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Neuroprotective effects and mechanisms of exercise in a chronic mouse model of Parkinson’s disease with moderate neurodegeneration</title></titleInfo><name type="personal"><namePart type="given">Yuen‐Sum</namePart><namePart type="family">Lau</namePart><affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gaurav</namePart><namePart type="family">Patki</namePart><affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kaberi</namePart><namePart type="family">Das‐Panja</namePart><affiliation>Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wei‐Dong</namePart><namePart type="family">Le</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, TX, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. Omar</namePart><namePart type="family">Ahmad</namePart><affiliation>Department of Occupational Therapy Education, Kansas University Medical Center, Kansas City, KS, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-04</dateIssued><edition>Received 30 September 2010, accepted 6 January 2011</edition><copyrightDate encoding="w3cdtf">2011</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">7</extent></physicalDescription><abstract lang="en">The protective impact of exercise on neurodegenerative processes has not been confirmed, and the mechanisms underlying the benefit of exercise have not been determined in human Parkinson’s disease or in chronic animal disease models. This research examined the long‐term neurological, behavioral, and mechanistic consequences of endurance exercise in experimental chronic parkinsonism. We used a chronic 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐induced mouse model of Parkinson’s disease with moderate neurodegeneration and examined the effects of treadmill exercise on movement and balance coordination, changes in dopamine neuron biomarkers, mitochondrial functions, and neurotrophic factor activities in the nigrostriatal system. The exercise results were compared with those of the control and sedentary chronic parkinsonian animals. After 18 weeks of exercise training in the chronic parkinsonian mice, we observed a significant deterrence in the loss of neuronal dopamine‐producing cells and other functional indicators. The impaired movement and balance incoordination in the chronic parkinsonian mice were also markedly reduced following exercise. Mechanistic investigations revealed that the neuronal and behavioral recovery produced by exercise in the chronic parkinsonian mice was associated with an improved mitochondrial function and an increase in the brain region‐specific levels of brain‐derived and glial cell line‐derived neurotrophic factors. Our findings indicate that exercise not only produces neuronal and mitochondrial protection, it also boosts nigrostriatal neurotrophic factor levels in the chronic parkinsonian mice with moderate neurodegeneration. Therefore, modifying lifestyle with increased exercise activity would be a non‐pharmacological neuroprotective approach for averting neurodegenerative processes, as demonstrated in experimental chronic parkinsonism.</abstract><subject lang="en"><genre>Keywords</genre><topic>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine parkinsonism</topic><topic>endurance exercise</topic><topic>mitochondrial dysfunction</topic><topic>neuroprotection</topic><topic>neurotrophic factor</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Figure S1. Nigrostriatal effects of 10 weeks of exercise in chronic MPD. Table S1. Summary and comparison of exercise studies in rodent models of PD. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer‐reviewed and may be re‐organized for online delivery, but are not copy‐edited or typeset by Wiley‐Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Figure S1. Nigrostriatal effects of 10 weeks of exercise in chronic MPD. Table S1. Summary and comparison of exercise studies in rodent models of PD. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer‐reviewed and may be re‐organized for online delivery, but are not copy‐edited or typeset by Wiley‐Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Figure S1. Nigrostriatal effects of 10 weeks of exercise in chronic MPD. Table S1. Summary and comparison of exercise studies in rodent models of PD. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer‐reviewed and may be re‐organized for online delivery, but are not copy‐edited or typeset by Wiley‐Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors.Supporting Info Item: Supporting info item - Supporting info item - Supporting info item - </note><subject><genre>article category</genre><topic>NEUROSYSTEMS</topic></subject><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1264</start><end>1274</end><total>11</total></extent></part></relatedItem><identifier type="istex">963389C1F0EAB819253624453753C00A4F447E29</identifier><identifier type="DOI">10.1111/j.1460-9568.2011.07626.x</identifier><identifier type="ArticleID">EJN7626</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2011 The Authors. European Journal of Neuroscience © 2011 Federation of European Neuroscience Societies and Blackwell Publishing Ltd</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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