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dc.rights.licenseopenen_US
dc.contributor.authorTOURNISSAC, Marine
dc.contributor.authorVANDAL, Milene
dc.contributor.authorTREMBLAY, Cyntia
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorBOURASSA, Philippe
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorVANCASSEL, Sylvie
dc.contributor.authorEMOND, Vincent
dc.contributor.authorGANGLOFF, Anne
dc.contributor.authorCALON, Frederic
dc.date.accessioned2021-09-21T08:08:06Z
dc.date.available2021-09-21T08:08:06Z
dc.date.issued2018
dc.identifier.issn2352-8737en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/112270
dc.description.abstractEnIntroduction High levels of plasmatic branched-chain amino acids (BCAA), commonly used as dietary supplements, are linked to metabolic risk factors for Alzheimer's disease (AD). BCAA directly influence amino acid transport to the brain and, therefore, neurotransmitter levels. We thus investigated the impact of BCAA on AD neuropathology in a mouse model. Methods 3xTg-AD mice were fed either a control diet or a high-fat diet from 6 to 18 months of age. For the last 2 months, dietary BCAA content was adjusted to high (+50%), normal (+0%), or low (−50%). Results Mice fed a BCAA-supplemented high-fat diet displayed higher tau neuropathology and only four out of 13 survived. Mice on the low-BCAA diet showed higher threonine and tryptophan cortical levels while performing better on the novel object recognition task. Discussion These preclinical data underscore a potential risk of combining high-fat and high BCAA consumption, and possible benefits from BCAA restriction in AD.
dc.language.isoENen_US
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subject.en3xTg-AD mice
dc.subject.enAlzheimer's disease
dc.subject.enBranched-chain amino acids
dc.subject.enDietary protein
dc.subject.enTau pathology
dc.title.enDietary intake of branched-chain amino acids in a mouse model of Alzheimer's disease: Effects on survival, behavior, and neuropathology
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.trci.2018.10.005en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed30560200en_US
bordeaux.journalAlzheimer's & Dementia: Translational Research & Clinical Interventionsen_US
bordeaux.page677-687en_US
bordeaux.volume4en_US
bordeaux.hal.laboratoriesNutriNeurO (Laboratoire de Nutrition et Neurobiologie Intégrée) - UMR 1286en_US
bordeaux.issue1en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINRAEen_US
bordeaux.teamPsychoneuroimmunologie et Nutrition: Approches expérimentales et cliniquesen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDCanadian Institutes of Health Researchen_US
bordeaux.identifier.funderIDCanada Foundation for Innovationen_US
bordeaux.identifier.funderIDFonds de Recherche du Québec - Santéen_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=Alzheimer's%20&%20Dementia:%20Translational%20Research%20&%20Clinical%20Interventions&rft.date=2018&rft.volume=4&rft.issue=1&rft.spage=677-687&rft.epage=677-687&rft.eissn=2352-8737&rft.issn=2352-8737&rft.au=TOURNISSAC,%20Marine&VANDAL,%20Milene&TREMBLAY,%20Cyntia&BOURASSA,%20Philippe&VANCASSEL,%20Sylvie&rft.genre=article


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