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dc.rights.licenseopenen_US
hal.structure.identifierLaboratoire des Maladies Neurodégénératives - UMR 9199 [LMN]
dc.contributor.authorBONVENTO, Gilles
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorOLIET, Stéphane
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorPANATIER, Aude
dc.date.accessioned2022-12-01T09:04:02Z
dc.date.available2022-12-01T09:04:02Z
dc.date.issued2022-05-03
dc.identifier.issn1550-4131en_US
dc.identifier.urioai:crossref.org:10.1016/j.cmet.2022.04.002
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/170441
dc.description.abstractEnRecent work from Bonvento and colleagues indicated that synaptic and memory deficits in early Alzheimer's disease (AD) are related to a shortage in L-serine production in astrocytes. Here, the authors, responding to correspondence from Chen and colleagues, discuss how this deficiency does not necessarily require a decrease in PHGDH expression and conclude that the primary event leading to lower serine production is more likely related to altered glycolytic flux in early AD than to PHGDH expression.
dc.language.isoENen_US
dc.sourcecrossref
dc.subject.enAlzheimer Disease / metabolism
dc.subject.enAstrocytes / metabolism
dc.subject.enGlycolysis
dc.subject.enHumans
dc.subject.enPhosphoglycerate Dehydrogenase / metabolism
dc.subject.enSerine / metabolism
dc.title.enGlycolysis-derived L-serine levels versus PHGDH expression in Alzheimer’s disease
dc.title.alternativeCell Metaben_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.cmet.2022.04.002en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed35508106en_US
bordeaux.journalCell Metabolismen_US
bordeaux.page654-655en_US
bordeaux.volume34en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - U1215en_US
bordeaux.issue5en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.teamRelations glie-neuroneen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcedissemin
hal.exportfalse
workflow.import.sourcedissemin
dc.rights.ccPas de Licence CCen_US
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