Mitochondrial respiratory chain function in multiple system atrophy
Identifieur interne : 005306 ( Main/Exploration ); précédent : 005305; suivant : 005307Mitochondrial respiratory chain function in multiple system atrophy
Auteurs : M. Gu [Royaume-Uni] ; M. T. Gash [Royaume-Uni] ; J. M. Cooper [Royaume-Uni] ; G. K. Wenning [Royaume-Uni] ; S. E. Daniel [Royaume-Uni] ; N. P. Quinn [Royaume-Uni] ; C. D. Marsden [Royaume-Uni] ; Schapira [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1997-05.
Descripteurs français
- Pascal (Inist)
- Wicri :
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (therapeutic use), Antiparkinson agent, Atrophy (pathology), Biochemistry, Blood Platelets, Brain (enzymology), Brain (pathology), Citrate (si)-Synthase (metabolism), Culture Techniques, Electron Transport, Human, Humans, Levodopa, Levodopa (administration & dosage), Levodopa (therapeutic use), Locus niger, L‐DOPA, Middle Aged, Mitochondria, Mitochondria (enzymology), Mitochondria (pathology), Multiple system atrophy, Nerve Degeneration, Parkinson Disease (diagnosis), Parkinson Disease (drug therapy), Pathogenesis, Platelet, Respiratory chain, Substantia Nigra, Toxicity, Treatment.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Levodopa.
- chemical , metabolism : Citrate (si)-Synthase.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- diagnosis : Parkinson Disease.
- drug therapy : Parkinson Disease.
- enzymology : Brain, Mitochondria.
- pathology : Atrophy, Brain, Mitochondria.
- Aged, Blood Platelets, Culture Techniques, Electron Transport, Humans, Middle Aged, Nerve Degeneration, Substantia Nigra.
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.
Url:
DOI: 10.1002/mds.870120323
Affiliations:
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Gu</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London</wicri:cityArea></affiliation></author><author><name sortKey="Gash, M T" sort="Gash, M T" uniqKey="Gash M" first="M. T." last="Gash">M. T. Gash</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London</wicri:cityArea></affiliation></author><author><name sortKey="Cooper, J M" sort="Cooper, J M" uniqKey="Cooper J" first="J. M." last="Cooper">J. M. Cooper</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London</wicri:cityArea></affiliation></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G. K." last="Wenning">G. K. Wenning</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology, Institute of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S. E." last="Daniel">S. E. Daniel</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Parkinson's Disease Society Brain Bank, London</wicri:cityArea></affiliation></author><author><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N. P." last="Quinn">N. P. Quinn</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology, Institute of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology, Institute of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London</wicri:cityArea></affiliation><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology, Institute of Neurology, London</wicri:cityArea></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>Aged</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Antiparkinson agent</term><term>Atrophy (pathology)</term><term>Biochemistry</term><term>Blood Platelets</term><term>Brain (enzymology)</term><term>Brain (pathology)</term><term>Citrate (si)-Synthase (metabolism)</term><term>Culture Techniques</term><term>Electron Transport</term><term>Human</term><term>Humans</term><term>Levodopa</term><term>Levodopa (administration & dosage)</term><term>Levodopa (therapeutic use)</term><term>Locus niger</term><term>L‐DOPA</term><term>Middle Aged</term><term>Mitochondria</term><term>Mitochondria (enzymology)</term><term>Mitochondria (pathology)</term><term>Multiple system atrophy</term><term>Nerve Degeneration</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (drug therapy)</term><term>Pathogenesis</term><term>Platelet</term><term>Respiratory chain</term><term>Substantia Nigra</term><term>Toxicity</term><term>Treatment</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Citrate (si)-Synthase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Brain</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Atrophy</term><term>Brain</term><term>Mitochondria</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Blood Platelets</term><term>Culture Techniques</term><term>Electron Transport</term><term>Humans</term><term>Middle Aged</term><term>Nerve Degeneration</term><term>Substantia Nigra</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Antiparkinsonien</term><term>Atrophie multisystématisée</term><term>Biochimie</term><term>Chaîne respiratoire</term><term>Homme</term><term>Locus niger</term><term>Lévodopa</term><term>Mitochondrie</term><term>Pathogénie</term><term>Thrombocyte</term><term>Toxicité</term><term>Traitement</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Biochimie</term><term>Homme</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><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Gu, M" sort="Gu, M" uniqKey="Gu M" first="M." last="Gu">M. Gu</name></region><name sortKey="Cooper, J M" sort="Cooper, J M" uniqKey="Cooper J" first="J. M." last="Cooper">J. M. Cooper</name><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S. E." last="Daniel">S. E. Daniel</name><name sortKey="Gash, M T" sort="Gash, M T" uniqKey="Gash M" first="M. T." last="Gash">M. T. Gash</name><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C. D." last="Marsden">C. D. Marsden</name><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N. P." last="Quinn">N. P. Quinn</name><name sortKey="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name><name sortKey="Schapira" sort="Schapira" uniqKey="Schapira" last="Schapira">Schapira</name><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G. K." last="Wenning">G. K. Wenning</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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