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<dc:title xml:lang="fr">Le développement de biomarqueurs et de la neuromodulation de précision dans la dépression : préciser les diagnostics, personnaliser les soins</dc:title>
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<dcterms:abstract xml:lang="fr">Ce corpus de thèse illustre le cheminement de notre réflexion sur l'utilisation des biomarqueurs dans la dépression, une pathologie dont les contours diagnostiques demeurent flous. Les premiers résultats d'études de neuroendocrinologie nous ont montré les limites des modèles "troubles" athéoriques et dimensionnels. Puisque la dépression affecte de nombreux systèmes neurologiques, il est difficile d'utiliser nos outils habituels pour identifier les atteintes qui pourraient servir d'hypothèses biologiques dans un modèle biomédical classique, comme nous l'avons fait pour la catatonie périodique. Le développement de biomarqueurs d'imagerie fiables à l'échelle du sujet unique, ainsi que de la rTMS de précision, nous ont permis de proposer une prise en charge individualisée en rTMS. Les résultats à l'échelle du groupe sont en faveur d'un lien entre les anomalies de perfusion cérébrale et dépression. Des analyses individuelles restent à faire. Elles pourront aboutir à une démarche de phénotypage inverse et a un rapprochement avec le modèle biomédical classique.</dcterms:abstract>
<dcterms:abstract xml:lang="en">This thesis illustrates the progress of our reflection on the use of biomarkers in depression, a pathology whose diagnostic contours remain unclear. Early results from neuroendocrinology studies have shown us the limitations of atheoretical and dimensional "disorder" models. Since depression affects many neurological systems, it is difficult to use our usual tools to identify impairments that could serve as biological hypotheses in a classical biomedical model, as we did for periodic catatonia. Hopefully, the development of reliable imaging biomarkers at the single-subject level, as well as precision rTMS, has allowed us to propose individualized rTMS management. The results at the group level are in favor of a link between cerebral perfusion abnormalities and depression. Individual analyses remain to be done. They could lead to an inverse phenotyping approach and a comparison with the classical biomedical model.</dcterms:abstract>
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