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dc.rights.licenseopenen_US
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorKOUBIYR, Ismail
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorYAMAMOTO, Takayuki
hal.structure.identifierCHU de Bordeaux Pellegrin [Bordeaux]
dc.contributor.authorBLYAU, Simon
hal.structure.identifierLaboratoire Bordelais de Recherche en Informatique [LaBRI]
dc.contributor.authorKAMROUI, Reda A
hal.structure.identifierLaboratoire Bordelais de Recherche en Informatique [LaBRI]
dc.contributor.authorMANSENCAL, Boris
IDREF: 228223601
hal.structure.identifierInstitut des Maladies Neurodégénératives [Bordeaux] [IMN]
dc.contributor.authorPLANCHE, Vincent
hal.structure.identifierInstitut des Maladies Neurodégénératives [Bordeaux] [IMN]
dc.contributor.authorPETIT, Laurent
hal.structure.identifierUniversity of Arizona
dc.contributor.authorSARANATHAN, Manojkumar
hal.structure.identifierUniversité Claude Bernard Lyon 1 [UCBL]
dc.contributor.authorCASEY, Romain
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorRUET, Aurelie
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorBROCHET, Bruno
hal.structure.identifierUniversitat Politècnica de València = Universitad Politecnica de Valencia = Polytechnic University of Valencia [UPV]
dc.contributor.authorMANJON, José V
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorDOUSSET, Vincent
hal.structure.identifierLaboratoire Bordelais de Recherche en Informatique [LaBRI]
dc.contributor.authorCOUPE, Pierrick
IDREF: 124687660
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorTOURDIAS, Thomas
dc.date.accessioned2025-04-24T14:27:41Z
dc.date.available2025-04-24T14:27:41Z
dc.date.issued2024-05
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/206404
dc.description.abstractEnBackground and Objectives Thalamic atrophy can be used as a proxy for neurodegeneration in multiple sclerosis (MS). Some data point toward thalamic nuclei that could be affected more than others. However, the dynamic of their changes during MS evolution and the mechanisms driving their differential alterations are still uncertain. Methods We paired a large cohort of 1,123 patients with MS with the same number of healthy controls, all scanned with conventional 3D-T1 MRI. To highlight the main atrophic regions at the thalamic nuclei level, we validated a segmentation strategy consisting of deep learning–based synthesis of sequences, which were used for automatic multiatlas segmentation. Then, through a lifespan–based approach, we could model the dynamics of the 4 main thalamic nuclei groups. Results All analyses converged toward a higher rate of atrophy for the posterior and medial groups compared with the anterior and lateral groups. We also demonstrated that focal MS white matter lesions were associated with atrophy of groups of nuclei when specifically located within the associated thalamocortical projections. The volumes of the most affected posterior group, but also of the anterior group, were better associated with clinical disability than the volume of the whole thalamus. Discussion These findings point toward the thalamic nuclei adjacent to the third ventricle as more susceptible to neurodegeneration during the entire course of MS through potentiation of disconnection effects by regional factors. Because this information can be obtained even from standard T1-weighted MRI, this paves the way toward such an approach for future monitoring of patients with MS. © 2024 American Academy of Neurology.
dc.description.sponsorshipApprentissage profond pour la volumétrie cérébrale : vers le BigData en neuroscienceen_US
dc.description.sponsorshipTranslational Research and Advanced Imaging Laboratoryen_US
dc.description.sponsorshipObservatoire Français de la Sclérose en Plaquesen_US
dc.language.isoENen_US
dc.subject.enAtrophy / pathology
dc.subject.enHumans
dc.subject.enMagnetic Resonance Imaging
dc.subject.enMultiple Sclerosis / pathology
dc.subject.enThalamic Nuclei / diagnostic imaging
dc.subject.enThalamus / diagnostic imaging
dc.subject.enThalamus / pathology
dc.title.enVulnerability of Thalamic Nuclei at CSF Interface During the Entire Course of Multiple Sclerosis
dc.title.alternativeNeurol Neuroimmunol Neuroinflammen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1212/NXI.0000000000200222en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed38635941en_US
bordeaux.journalNeurology Neuroimmunology & Neuroinflammationen_US
bordeaux.volume11en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - U1215en_US
bordeaux.issue3en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.institutionCNRS
bordeaux.teamRelations glie-neuroneen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDMinistère de l'Enseignement Supérieur et de la Recherche Scientifiqueen_US
bordeaux.identifier.funderIDMinisterio de Ciencia e Innovaciónen_US
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Neurology%20Neuroimmunology%20&%20Neuroinflammation&rft.date=2024-05&rft.volume=11&rft.issue=3&rft.au=KOUBIYR,%20Ismail&YAMAMOTO,%20Takayuki&BLYAU,%20Simon&KAMROUI,%20Reda%20A&MANSENCAL,%20Boris&rft.genre=article


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