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.
English descriptors
- 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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<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>
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<affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>University Department of Clinical Neurology, Institute of Neurology, London, England</unparsedAffiliation>
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<affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Parkinson's Disease Society Brain Bank, London, England</unparsedAffiliation>
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<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>
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<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>
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<!--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>
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<titleInfo type="abbreviated" lang="en"><title>MITOCHONDRIAL RESPIRATORY CHAIN FUNCTION IN MSA</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mitochondrial respiratory chain function in multiple system atrophy</title>
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<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>
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</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>
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<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>
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</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>
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<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>
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<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>
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<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>
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<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<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>
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<titleInfo type="abbreviated"><title>Mov. Disord.</title>
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<topic>Article</topic>
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<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>
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<detail type="issue"><caption>no.</caption>
<number>3</number>
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<extent unit="pages"><start>418</start>
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<identifier type="DOI">10.1002/mds.870120323</identifier>
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<accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 Movement Disorder Society</accessCondition>
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