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dc.rights.licenseopenen_US
hal.structure.identifierUniversité Laval [Québec] [ULaval]
hal.structure.identifierInstitut sur la Nutrition et les Aliments Fonctionnels [université Laval, Québec] [INAF]
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorBIYONG, Essi F.
dc.contributor.authorTREMBLAY, Cyntia
dc.contributor.authorLECLERC, Manon
dc.contributor.authorCARON, Vicky
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorALFOS, Serge
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorHELBLING, Jean-Christophe
dc.contributor.authorRODRIGUEZ, Lea
dc.contributor.authorPERNET, Vincent
dc.contributor.authorBENNETT, David A.
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorPALLET, Veronique
dc.contributor.authorCALON, Frederic
dc.date.accessioned2023-06-08T11:39:19Z
dc.date.available2023-06-08T11:39:19Z
dc.date.issued2021-12-01
dc.identifier.issn0969-9961en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/182537
dc.description.abstractEnBackground Vitamin A (VitA), via its active metabolite retinoic acid (RA), is critical for the maintenance of memory function with advancing age. Although its role in Alzheimer's disease (AD) is not well understood, data suggest that impaired brain VitA signaling is associated with the accumulation of β-amyloid peptides (Aβ), and could thus contribute to the onset of AD. Methods We evaluated the protective action of a six-month-long dietary VitA-supplementation (20 IU/g), starting at 8 months of age, on the memory and the neuropathology of the 3xTg-AD mouse model of AD (n = 11-14/group; including 4–6 females and 7–8 males). We also measured protein levels of Retinoic Acid Receptor β (RARβ) and Retinoid X Receptor γ (RXRγ) in homogenates from the inferior parietal cortex of 60 participants of the Religious Orders study (ROS) divided in three groups: no cognitive impairment (NCI) (n = 20), mild cognitive impairment (MCI) (n = 20) and AD (n = 20). Results The VitA-enriched diet preserved spatial memory of 3xTg-AD mice in the Y maze. VitA-supplementation affected hippocampal RXR expression in an opposite way according to sex by tending to increase in males and decrease in females their mRNA expression. VitA-enriched diet also reduced the amount of hippocampal Aβ40 and Aβ42, as well as the phosphorylation of tau protein at sites Ser396/Ser404 (PHF-1) in males. VitA-supplementation had no effect on tau phosphorylation in females but worsened their hippocampal Aβ load. However, the expression of Rxr-β in the hippocampus was negatively correlated with the amount of both soluble and insoluble Aβ in both males and females. Western immunoblotting in the human cortical samples of the ROS study did not reveal differences in RARβ levels. However, it evidenced a switch from a 60-kDa-RXRγ to a 55-kDa-RXRγ in AD, correlating with ante mortem cognitive decline and the accumulation of neuritic plaques in the brain cortex. Conclusion Our data suggest that (i) an altered expression of RXRs receptors is a contributor to β-amyloid pathology in both humans and 3xTg-AD mice, (ii) a chronic exposure of 3xTg-AD mice to a VitA-enriched diet may be protective in males, but not in females.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.en3xTg-AD mouse
dc.subject.enAging
dc.subject.enAlzheimer's disease
dc.subject.enAmyloid
dc.subject.enDiet
dc.subject.enPrevention
dc.subject.enRXRs
dc.subject.enSex
dc.subject.enVitamin A
dc.title.enRole of Retinoid X Receptors (RXRs) and dietary vitamin A in Alzheimer's disease: Evidence from clinicopathological and preclinical studies
dc.title.alternativeNeurobiology of Diseaseen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.nbd.2021.105542en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed34737043en_US
bordeaux.journalNeurobiology of Diseaseen_US
bordeaux.page105542en_US
bordeaux.volume161en_US
bordeaux.hal.laboratoriesNutriNeuro (Laboratoire de Nutrition et Neurobiologie Intégrée) - UMR 1286en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINRAEen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDConseil Régional Aquitaineen_US
hal.exportfalse
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Neurobiology%20of%20Disease&rft.date=2021-12-01&rft.volume=161&rft.spage=105542&rft.epage=105542&rft.eissn=0969-9961&rft.issn=0969-9961&rft.au=BIYONG,%20Essi%20F.&TREMBLAY,%20Cyntia&LECLERC,%20Manon&CARON,%20Vicky&ALFOS,%20Serge&rft.genre=article


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