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dc.rights.licenseopenen_US
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorMARIE, Anais
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorLEROY, Julien
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorPALLET, Veronique
ORCID: 0000-0002-9078-3269
IDREF: 066841763
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorVANCASSEL, Sylvie
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorBOSCH BOUJU, Clementine
ORCID: 0000-0001-8869-768X
IDREF: 156530244
dc.date.accessioned2021-09-21T07:49:12Z
dc.date.available2021-09-21T07:49:12Z
dc.date.issued2019-04
dc.date.conference2019-04-28
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/112266
dc.descriptionPosteren_US
dc.description.abstractEnParkinson’s disease (PD) is a brain disease caused by a loss of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to strong motor impairments. Vitamin A, through the action of its active metabolite retinoic acid (RA), is involved in the development, differentiation and protection of SNc dopaminergic neurons. However, the bioavailability of retinoic acid in the brain decreases with aging. Prior reports suggest that altered vitamin A signaling is implicated in the etiology of Parkinson’s disease, though the mechanisms are poorly understood. Here we hypothesize that nutritional supplementation with vitamin A may reduce dopaminergic cells loss by increasing RA levels in the brain, thus delaying the progression of the disease. We showed that rats deprived of vitamin A became progressively impaired in their motor functions and were unable to perform correctly the rotarod test after thirteen weeks of deprivation. However, locomotor functions were improved after just three weeks of vitamin A supplementation. To assess the effect of vitamin A supplementation, we modeled Parkinson’s disease in rat. Dopaminergic neurons were selectively deleted with unilateral injection of 6-hydroxydopamine (6-OHDA) toxin into rat’s striatum. Rats fed a vitamin A supplemented diet (20UI/g) for five weeks prior to the toxin injection exhibited an improvement in rotarod test compared to rats fed with control diet (5UI/g). Degeneration of dopaminergic terminals was assessed with stereological analysis of tyrosine hydroxylase staining in the striatum. Finally, dopamine levels in striatum were measured with HPLC. These preliminary data established the link between dietary vitamin A and dopaminergic system in PD. Future work will focus on establishing its underlying mechanisms and molecular basis.
dc.language.isoENen_US
dc.title.enImplication of vitamin A in neuroprotection of dopaminergic neurons in a rat model of Parkinson's disease
dc.typeAutre communication scientifique (congrès sans actes - poster - séminaire...)en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
bordeaux.hal.laboratoriesNutriNeurO (Laboratoire de Nutrition et Neurobiologie Intégrée) - UMR 1286en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINRAEen_US
bordeaux.conference.titleIBAGS Meetingen_US
bordeaux.countryfren_US
bordeaux.teamPsychoneuroimmunologie et Nutrition: Approches expérimentales et cliniquesen_US
bordeaux.teamNutrition, mémoire et glucocorticoïdesen_US
bordeaux.conference.cityBiarritzen_US
bordeaux.peerReviewedouien_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.date=2019-04&rft.au=MARIE,%20Anais&LEROY,%20Julien&PALLET,%20Veronique&VANCASSEL,%20Sylvie&BOSCH%20BOUJU,%20Clementine&rft.genre=conference


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