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     <dc:title xml:lang="fr">L’influence du microbiote intestinal dans la maladie de Parkinson</dc:title>
     <dcterms:alternative xml:lang="en">The influence of the intestinal microbiota in Parkinson's disease</dcterms:alternative>
     <dc:subject xml:lang="fr">Microbiote intestinal</dc:subject><dc:subject xml:lang="fr">dysbiose</dc:subject><dc:subject xml:lang="fr">flore intestinal</dc:subject><dc:subject xml:lang="fr">Parkinson</dc:subject><dc:subject xml:lang="fr">dopamine</dc:subject>
     <dc:subject xml:lang="en">Gut microbiota</dc:subject><dc:subject xml:lang="en">dysbiosis</dc:subject><dc:subject xml:lang="en">gut flora</dc:subject><dc:subject xml:lang="en">Parkinson</dc:subject><dc:subject xml:lang="en">dopamine</dc:subject><tef:sujetRameau><tef:vedetteRameauNomCommun>
						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="176309519">Flore intestinale</tef:elementdEntree>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="027794245">Maladie de Parkinson</tef:elementdEntree><tef:subdivision autoriteSource="Sudoc" type="subdivisionDeSujet" autoriteExterne="027589838">Thérapeutique</tef:subdivision>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="199682852">Dysbiose</tef:elementdEntree>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="031018726">Probiotiques</tef:elementdEntree>
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						<tef:elementdEntree autoriteSource="Sudoc" autoriteExterne="232929300">Transplantation de microbiote fécal </tef:elementdEntree>
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     <dcterms:abstract xml:lang="fr">Les avancées thérapeutiques majeurs de ces dernières années concernant la maladie de Parkinson, notamment avec les avancées scientifiques sur la communication bidirectionnelle entre le système nerveux central et le microbiote intestinal, représentent un enjeu majeur de santé public. La dérégulation de cet axe dans la maladie de Parkinson pourrait être associée à des manifestations gastro-intestinales précédant les symptômes moteurs, ainsi qu’à la pathogenèse de la maladie de Parkinson elle-même, ce qui évoquerait une hypothèse de processus pathologique qui se propage de l’intestin au cerveau. L’objectif de cette thèse est de montrer comment le microbiote intestinal permet, grâce à sa composition et ses métabolites, d’influencer sur la pathogénèse et les symptômes de la maladie de Parkinson. La littérature scientifique grandissante et récente va me permettre de donner des réponses à ce sujet en exposant différentes parties : le microbiote intestinal, la maladie de Parkinson, les modulations du microbiote intestinal chez les patients et leurs impacts, les corrélations entre les aspects cliniques et le changement de composition du microbiote ou encore les perspectives thérapeutiques futures avec les probiotiques et la transplantation fécale.</dcterms:abstract>
     <dcterms:abstract xml:lang="en">The major therapeutic advances of the last few years concerning Parkinson's disease, especially with the scientific advances on the bidirectional communication between the central nervous system and the intestinal microbiota, represent a major public health issue. The deregulation of this axis in Parkinson's disease could be associated with gastrointestinal manifestations preceding the motor symptoms, as well as with the pathogenesis of Parkinson's disease itself, which would evoke a hypothesis of a pathological process that spreads from the gut to the brain. The objective of this thesis is to show how the gut microbiota, through its composition and metabolites, can influence the pathogenesis and symptoms of Parkinson's disease. The growing and recent scientific literature will allow me to give answers to this subject by exposing different parts: the intestinal microbiota, the Parkinson's disease, the modulations of the intestinal microbiota and their impacts, the correlations between the clinical aspects and the change of composition of the microbiota or the future therapeutic perspectives with probiotics and fecal transplantation.</dcterms:abstract>
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       <tef:nom>Potier</tef:nom>
       <tef:prenom>Guillaume</tef:prenom>
       
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