Maladie de Parkinson: mécanismes physiopathologiques et effets du piribédil
Identifieur interne : 000009 ( Main/Corpus ); précédent : 000008; suivant : 000010Maladie de Parkinson: mécanismes physiopathologiques et effets du piribédil
Auteurs : Peter JennerSource :
- Journal of Neurology [ 0340-5354 ] ; 1993-01-01.
Abstract
Résumé: Lors de la maladie de Parkinson, la dégénérescence des cellules dopaminergiques situées dans la zona compacta du locus niger reste de cause inconnue. La capacité de la 1-méthyl-4-phényl-1,2,3,6, tétrahydropyridine (MPTP), toxine sélective du locus niger, à détruire sélectivement les cellules dopaminergiques de ce noyau (via son métabolite MPP+) en inhibant le complexe I du cycle énergétique mitochondrial, pourrait représenter un début d'explication. En effet, des études récentes effectuées post-mortem sur le tissu cérébral ont suggéré l'existence, au cours de la maladie de Parkinson, d'un processus toxique évolutif affectant le locus niger et entraînant un excès de peroxydation lipidique. Ce processus semble également impliquer une interruption du fonctionnement mitochondrial, avec une hyperactivité de la superoxyde dismutase mitochondriale ainsi que des anomalies du complexe I. Ces modifications pourraient à leur tour être liées à une augmentation sélective de la teneur totale en fer du locus niger, couplée à une diminution généralisée de la teneur cérébrale en ferritine. Le piribédil est utilisé dans le traitement symptomatique de la maladie de Parkinson; il est particulièrement efficace sur le tremblement. Le piribédil se comporte (ainsi que ses métabolites) comme un agoniste des récepteurs dopaminergiques D2. Toutefois nos travaux montrent que, contrairement aux autres agonistes dopaminergiques, le piribédil interagit in vivo avec les récepteurs dopaminergiques du locus niger et du nucleus accumbens, mais non avec ceux du striatum. Lors de la maladie de Parkinson, les effets bénéfiques du piribédil peuvent être limités par la survenue de nausées et de somnolence. En effet, chez le primate traité par le MPTP, le piribédil corrige les déficits moteurs mais peut entraîner des effets secondaires gênants. Toutefois, un traitement préalable par la dompéridone, antagoniste périphérique des récepteurs dopaminergiques, prévient ces effets indésirables et le piribédil induit une correction profonde et prolongée de toutes les composantes du syndrome moteur. Ces résultats suggèrent qu'en association avec la dompéridone, le piribédil pourrait représenter une monothérapie efficace de la maladie de Parkinson.
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DOI: 10.1007/BF00879099
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La capacité de la 1-méthyl-4-phényl-1,2,3,6, tétrahydropyridine (MPTP), toxine sélective du locus niger, à détruire sélectivement les cellules dopaminergiques de ce noyau (via son métabolite MPP+) en inhibant le complexe I du cycle énergétique mitochondrial, pourrait représenter un début d'explication. En effet, des études récentes effectuées post-mortem sur le tissu cérébral ont suggéré l'existence, au cours de la maladie de Parkinson, d'un processus toxique évolutif affectant le locus niger et entraînant un excès de peroxydation lipidique. Ce processus semble également impliquer une interruption du fonctionnement mitochondrial, avec une hyperactivité de la superoxyde dismutase mitochondriale ainsi que des anomalies du complexe I. Ces modifications pourraient à leur tour être liées à une augmentation sélective de la teneur totale en fer du locus niger, couplée à une diminution généralisée de la teneur cérébrale en ferritine. Le piribédil est utilisé dans le traitement symptomatique de la maladie de Parkinson; il est particulièrement efficace sur le tremblement. Le piribédil se comporte (ainsi que ses métabolites) comme un agoniste des récepteurs dopaminergiques D2. Toutefois nos travaux montrent que, contrairement aux autres agonistes dopaminergiques, le piribédil interagit in vivo avec les récepteurs dopaminergiques du locus niger et du nucleus accumbens, mais non avec ceux du striatum. Lors de la maladie de Parkinson, les effets bénéfiques du piribédil peuvent être limités par la survenue de nausées et de somnolence. En effet, chez le primate traité par le MPTP, le piribédil corrige les déficits moteurs mais peut entraîner des effets secondaires gênants. Toutefois, un traitement préalable par la dompéridone, antagoniste périphérique des récepteurs dopaminergiques, prévient ces effets indésirables et le piribédil induit une correction profonde et prolongée de toutes les composantes du syndrome moteur. Ces résultats suggèrent qu'en association avec la dompéridone, le piribédil pourrait représenter une monothérapie efficace de la maladie de Parkinson.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>Peter Jenner</name><affiliations><json:string>Parkinson's Disease Society Experimental Research Laboratories, Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, SW3 6LX, London, UK</json:string></affiliations></json:item></author><articleId><json:string>Art2</json:string><json:string>BF00879099</json:string></articleId><language><json:string>fre</json:string></language><abstract>Résumé: Lors de la maladie de Parkinson, la dégénérescence des cellules dopaminergiques situées dans la zona compacta du locus niger reste de cause inconnue. La capacité de la 1-méthyl-4-phényl-1,2,3,6, tétrahydropyridine (MPTP), toxine sélective du locus niger, à détruire sélectivement les cellules dopaminergiques de ce noyau (via son métabolite MPP+) en inhibant le complexe I du cycle énergétique mitochondrial, pourrait représenter un début d'explication. En effet, des études récentes effectuées post-mortem sur le tissu cérébral ont suggéré l'existence, au cours de la maladie de Parkinson, d'un processus toxique évolutif affectant le locus niger et entraînant un excès de peroxydation lipidique. Ce processus semble également impliquer une interruption du fonctionnement mitochondrial, avec une hyperactivité de la superoxyde dismutase mitochondriale ainsi que des anomalies du complexe I. Ces modifications pourraient à leur tour être liées à une augmentation sélective de la teneur totale en fer du locus niger, couplée à une diminution généralisée de la teneur cérébrale en ferritine. Le piribédil est utilisé dans le traitement symptomatique de la maladie de Parkinson; il est particulièrement efficace sur le tremblement. Le piribédil se comporte (ainsi que ses métabolites) comme un agoniste des récepteurs dopaminergiques D2. Toutefois nos travaux montrent que, contrairement aux autres agonistes dopaminergiques, le piribédil interagit in vivo avec les récepteurs dopaminergiques du locus niger et du nucleus accumbens, mais non avec ceux du striatum. Lors de la maladie de Parkinson, les effets bénéfiques du piribédil peuvent être limités par la survenue de nausées et de somnolence. En effet, chez le primate traité par le MPTP, le piribédil corrige les déficits moteurs mais peut entraîner des effets secondaires gênants. Toutefois, un traitement préalable par la dompéridone, antagoniste périphérique des récepteurs dopaminergiques, prévient ces effets indésirables et le piribédil induit une correction profonde et prolongée de toutes les composantes du syndrome moteur. 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La capacité de la 1-méthyl-4-phényl-1,2,3,6, tétrahydropyridine (MPTP), toxine sélective du locus niger, à détruire sélectivement les cellules dopaminergiques de ce noyau (via son métabolite MPP+) en inhibant le complexe I du cycle énergétique mitochondrial, pourrait représenter un début d'explication. En effet, des études récentes effectuées post-mortem sur le tissu cérébral ont suggéré l'existence, au cours de la maladie de Parkinson, d'un processus toxique évolutif affectant le locus niger et entraînant un excès de peroxydation lipidique. Ce processus semble également impliquer une interruption du fonctionnement mitochondrial, avec une hyperactivité de la superoxyde dismutase mitochondriale ainsi que des anomalies du complexe I. Ces modifications pourraient à leur tour être liées à une augmentation sélective de la teneur totale en fer du locus niger, couplée à une diminution généralisée de la teneur cérébrale en ferritine. Le piribédil est utilisé dans le traitement symptomatique de la maladie de Parkinson; il est particulièrement efficace sur le tremblement. Le piribédil se comporte (ainsi que ses métabolites) comme un agoniste des récepteurs dopaminergiques D2. Toutefois nos travaux montrent que, contrairement aux autres agonistes dopaminergiques, le piribédil interagit in vivo avec les récepteurs dopaminergiques du locus niger et du nucleus accumbens, mais non avec ceux du striatum. Lors de la maladie de Parkinson, les effets bénéfiques du piribédil peuvent être limités par la survenue de nausées et de somnolence. En effet, chez le primate traité par le MPTP, le piribédil corrige les déficits moteurs mais peut entraîner des effets secondaires gênants. Toutefois, un traitement préalable par la dompéridone, antagoniste périphérique des récepteurs dopaminergiques, prévient ces effets indésirables et le piribédil induit une correction profonde et prolongée de toutes les composantes du syndrome moteur. 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La capacité de la 1-méthyl-4-phényl-1,2,3,6, tétrahydropyridine (MPTP), toxine sélective du locus niger, à détruire sélectivement les cellules dopaminergiques de ce noyau (via son métabolite MPP<Superscript>+</Superscript>) en inhibant le complexe I du cycle énergétique mitochondrial, pourrait représenter un début d'explication. En effet, des études récentes effectuées post-mortem sur le tissu cérébral ont suggéré l'existence, au cours de la maladie de Parkinson, d'un processus toxique évolutif affectant le locus niger et entraînant un excès de peroxydation lipidique. Ce processus semble également impliquer une interruption du fonctionnement mitochondrial, avec une hyperactivité de la superoxyde dismutase mitochondriale ainsi que des anomalies du complexe I. Ces modifications pourraient à leur tour être liées à une augmentation sélective de la teneur totale en fer du locus niger, couplée à une diminution généralisée de la teneur cérébrale en ferritine. Le piribédil est utilisé dans le traitement symptomatique de la maladie de Parkinson; il est particulièrement efficace sur le tremblement. Le piribédil se comporte (ainsi que ses métabolites) comme un agoniste des récepteurs dopaminergiques D<Subscript>2</Subscript>. Toutefois nos travaux montrent que, contrairement aux autres agonistes dopaminergiques, le piribédil interagit in vivo avec les récepteurs dopaminergiques du locus niger et du nucleus accumbens, mais non avec ceux du striatum. Lors de la maladie de Parkinson, les effets bénéfiques du piribédil peuvent être limités par la survenue de nausées et de somnolence. En effet, chez le primate traité par le MPTP, le piribédil corrige les déficits moteurs mais peut entraîner des effets secondaires gênants. Toutefois, un traitement préalable par la dompéridone, antagoniste périphérique des récepteurs dopaminergiques, prévient ces effets indésirables et le piribédil induit une correction profonde et prolongée de toutes les composantes du syndrome moteur. Ces résultats suggèrent qu'en association avec la dompéridone, le piribédil pourrait représenter une monothérapie efficace de la maladie de Parkinson.</Para></Abstract><KeywordGroup Language="Fr"><Heading>Mots clés</Heading><Keyword>Maladie de Parkinson</Keyword><Keyword>Etudes post-mortem</Keyword><Keyword>Perturbations mitochondriales</Keyword><Keyword>Piribédil</Keyword><Keyword>MPTP</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="fr"><title>Maladie de Parkinson: mécanismes physiopathologiques et effets du piribédil</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="fr"><title>Maladie de Parkinson: mécanismes physiopathologiques et effets du piribédil</title></titleInfo><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Jenner</namePart><affiliation>Parkinson's Disease Society Experimental Research Laboratories, Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, SW3 6LX, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateIssued encoding="w3cdtf">1993-01-01</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">fr</languageTerm><languageTerm type="code" authority="iso639-2b">fre</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="fr">Résumé: Lors de la maladie de Parkinson, la dégénérescence des cellules dopaminergiques situées dans la zona compacta du locus niger reste de cause inconnue. La capacité de la 1-méthyl-4-phényl-1,2,3,6, tétrahydropyridine (MPTP), toxine sélective du locus niger, à détruire sélectivement les cellules dopaminergiques de ce noyau (via son métabolite MPP+) en inhibant le complexe I du cycle énergétique mitochondrial, pourrait représenter un début d'explication. En effet, des études récentes effectuées post-mortem sur le tissu cérébral ont suggéré l'existence, au cours de la maladie de Parkinson, d'un processus toxique évolutif affectant le locus niger et entraînant un excès de peroxydation lipidique. Ce processus semble également impliquer une interruption du fonctionnement mitochondrial, avec une hyperactivité de la superoxyde dismutase mitochondriale ainsi que des anomalies du complexe I. Ces modifications pourraient à leur tour être liées à une augmentation sélective de la teneur totale en fer du locus niger, couplée à une diminution généralisée de la teneur cérébrale en ferritine. Le piribédil est utilisé dans le traitement symptomatique de la maladie de Parkinson; il est particulièrement efficace sur le tremblement. Le piribédil se comporte (ainsi que ses métabolites) comme un agoniste des récepteurs dopaminergiques D2. Toutefois nos travaux montrent que, contrairement aux autres agonistes dopaminergiques, le piribédil interagit in vivo avec les récepteurs dopaminergiques du locus niger et du nucleus accumbens, mais non avec ceux du striatum. Lors de la maladie de Parkinson, les effets bénéfiques du piribédil peuvent être limités par la survenue de nausées et de somnolence. En effet, chez le primate traité par le MPTP, le piribédil corrige les déficits moteurs mais peut entraîner des effets secondaires gênants. Toutefois, un traitement préalable par la dompéridone, antagoniste périphérique des récepteurs dopaminergiques, prévient ces effets indésirables et le piribédil induit une correction profonde et prolongée de toutes les composantes du syndrome moteur. 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