33 results on '"Alfos S"'
Search Results
2. Adult-Onset Hypothyroidism Induces the Amyloidogenic Pathway of Amyloid Precursor Protein Processing in the Rat Hippocampus
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Ghenimi, N., Alfos, S., Redonnet, A., Higueret, P., Pallet, V., and Enderlin, V.
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- 2010
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3. Differential effect of retinoic acid and triiodothyronine on the age-related hypo-expression of neurogranin in rat
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Féart, C., Mingaud, F., Enderlin, V., Husson, M., Alfos, S., Higueret, P., and Pallet, V.
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- 2005
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4. Expression of neurogranin and neuromodulin is affected in the striatum of vitamin A-deprived rats
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Husson, M, Enderlin, V, Alfos, S, Boucheron, C, Pallet, V, and Higueret, P
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- 2004
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5. Adult-onset hypothyroidism induces the amyloidogenic pathway of APP processing in the rat hippocampus
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Ghenimi Rahab, N., primary, Alfos, S., additional, Redonnet, A., additional, Higueret, P., additional, Pallet, V., additional, and Enderlin, V., additional
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- 2010
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6. Aging affects the retinoic acid and the triiodothyronine nuclear receptor mRNA expression in human peripheral blood mononuclear cells
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Feart, C, primary, Pallet, V, additional, Boucheron, C, additional, Higueret, D, additional, Alfos, S, additional, Letenneur, L, additional, Dartigues, J F, additional, and Higueret, P, additional
- Published
- 2005
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7. Vitamin A Deficiency Decreases the Expression of RARβ and RXRβ/γ in Adult Mouse Brain: Effect of RA Administration
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Enderlin, V., primary, Higueret, D., additional, Alfos, S., additional, Husson, M., additional, Jaffard, R., additional, Higueret, P., additional, and Pallet, V., additional
- Published
- 2000
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8. Aging decreases the abundance of retinoic acid (RAR) and triiodothyronine (TR) nuclear receptor mRNA in rat brain: effect of the administration of retinoids
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Enderlin, V, primary, Alfos, S, additional, Pallet, V, additional, Garcin, H, additional, Azaı̈s-Braesco, V, additional, Jaffard, R, additional, and Higueret, P, additional
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- 1997
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9. A high-fat diet induces lower expression of retinoid receptors and their target genes GAP-43/neuromodulin and RC3/neurogranin in the rat brain.
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Buaud B, Esterle L, Vaysse C, Alfos S, Combe N, Higueret P, and Pallet V
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- 2010
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10. Chronic ethanol consumption increases the amount of mRNA for retinoic acid and triiodothyronine receptors in mouse brain
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Alfos, S., Higueret, P., Pallet, V., Higueret, D., Garcin, H., and Jaffard, R.
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- 1996
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11. Age-related decreases in mRNA for brain nuclear receptors and target genes are reversed by retinoic acid treatment
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Enderlin, V., Pallet, V., Alfos, S., Dargelos, E., Jaffard, R., Garcin, H., and Higueret, P.
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- 1997
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12. [In vitro cell cultures in acute leukaemia (author's transl)]
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Lourdes Florensa, Nomdedeu Tobella B, Gallego Alfos S, Brugues Riera R, Jl, Vives Corrons, and Rozman C
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Adult ,Male ,Leukemia ,Adolescent ,Bone Marrow Cells ,Middle Aged ,Hematopoietic Stem Cells ,Prognosis ,Colony-Stimulating Factors ,Acute Disease ,Humans ,Female ,Cell Division ,Cells, Cultured ,Aged
13. Retinoids modulate the binding capacity of the glucocorticoid receptor and its translocation from cytosol to nucleus in liver cells
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Audouin-Chevallier, I., Pallet, V., Coustaut, M., and Alfos, S.
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- 1995
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14. Impact of dietary vitamin A on striatal function in adult rats.
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Marie A, Kinet R, Helbling JC, Darricau M, Alfos S, Di Miceli M, Angelo MF, Foury A, Richard E, Trifilieff P, Mallet NP, and Bosch-Bouju C
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- Rats, Animals, Rats, Sprague-Dawley, Retinoids, Diet, Vitamin A, Corpus Striatum
- Abstract
The striatum is a brain structure involved in the control of voluntary movement. Striatum contains high amounts of retinoic acid, the active metabolite of vitamin A, as well as retinoid receptors, RARβ and RXRγ. Previous studies revealed that disruption of retinoid signaling initiated during development is deleterious for striatal physiology and related motor functions. However, the alteration of retinoid signaling, and the importance of vitamin A supply during adulthood on striatal physiology and function has never been established. In the present study, we investigated the impact of vitamin A supply on striatal function. Adult Sprague-Dawley rats were fed with three specific diets, either sub-deficient, sufficient, or enriched in vitamin A (0.4, 5, and 20 international units [IU] of retinol per g of diet, respectively) for 6 months. We first validated that vitamin A sub-deficient diet in adult rats constitutes a physiological model of retinoid signaling reduction in the striatum. We then revealed subtle alterations of fine motor skills in sub-deficient rats using a new behavioral apparatus specifically designed to test forepaw reach-and-grasp skills relying on striatal function. Finally, we showed using qPCR analysis and immunofluorescence that the striatal dopaminergic system per se was not affected by vitamin A sub-deficiency at adult age. Rather, cholinergic synthesis in the striatum and μ-opioid receptor expression in striosomes sub-territories were the most affected by vitamin A sub-deficiency starting at adulthood. Taken together these results revealed that retinoid signaling alteration at adulthood is associated with motor learning deficits together with discrete neurobiological alterations in the striatum., (© 2023 Federation of American Societies for Experimental Biology.)
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- 2023
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15. Neuronal morphology and synaptic plasticity in the hippocampus of vitamin A deficient rats.
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Dumetz F, Ginieis R, Bure C, Marie A, Alfos S, Pallet V, and Bosch-Bouju C
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- Animals, Chromatography, Liquid, Hippocampus metabolism, Male, Neuronal Plasticity, Neurons, Rats, Rats, Wistar, Tandem Mass Spectrometry, Vitamin A
- Abstract
Vitamin A (retinol) and related retinoids are micronutrients provided by food. Retinol derivatives are growth factors important for development, cell differentiation and tissue homeostasis, especially in the brain. Objective : The hippocampus is a pivotal brain structure for learning and memory and hippocampal-dependent memory is highly sensitive to retinoids action. However, the underlying mechanisms are still unclear. In this study, we characterized the impact of vitamin A deficiency on memory and neuronal plasticity, focusing on the CA1 region of the hippocampus in rats. Methods : Weaned male Wistar rats were fed a control (5 UI/g) or deficient vitamin A diet (0 UI/g) for 10 weeks. The effect of vitamin A supplementation (20 UI/g) for 3 weeks was also tested. Memory performances were assessed in the Y-maze ( n = 24-30/group), retinoic acid levels were measured (LC-MS/MS) in the serum and in the hippocampus ( n = 5/group), CA1 neuronal architecture was analyzed with Golgi staining ( n = 17-20 neurons/group) and electrophysiological patch-clamp recordings were performed on hippocampal brain slices ( n = 6-11/group). Results : Vitamin A deficiency from weaning significantly lowered hippocampal levels of retinoic acid, reduced dendritic length and branching of CA1 pyramidal neurons and decreased spontaneous glutamatergic synaptic events and synaptic plasticity. When replenishment with moderate dose of dietary vitamin A for 3 weeks was done, most of the synaptic and morphological alterations were absent. Conclusion : This study provides new mechanistic insight to understand the critical role of retinoic acid in hippocampal function.
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- 2022
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16. Preventive Vitamin A Supplementation Improves Striatal Function in 6-Hydroxydopamine Hemiparkinsonian Rats.
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Marie A, Leroy J, Darricau M, Alfos S, De Smedt-Peyrusse V, Richard E, Vancassel S, and Bosch-Bouju C
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Background: The mechanisms leading to a loss of dopaminergic (DA) neurons from the substantia nigra pars compacta (SNc) in Parkinson's disease (PD) have multifactorial origins. In this context, nutrition is currently investigated as a modifiable environmental factor for the prevention of PD. In particular, initial studies revealed the deleterious consequences of vitamin A signaling failure on dopamine-related motor behaviors. However, the potential of vitamin A supplementation itself to prevent neurodegeneration has not been established yet., Objective: The hypothesis tested in this study is that preventive vitamin A supplementation can protect DA neurons in a rat model of PD., Methods: The impact of a 5-week preventive supplementation with vitamin A (20 IU/g of diet) was measured on motor and neurobiological alterations induced by 6-hydroxydopamine (6-OHDA) unilateral injections in the striatum of rats. Rotarod, step test and cylinder tests were performed up to 3 weeks after the lesion. Post-mortem analyses (retinol and monoamines dosages, western blots, immunofluorescence) were performed to investigate neurobiological processes., Results: Vitamin A supplementation improved voluntary movements in the cylinder test. In 6-OHDA lesioned rats, a marked decrease of dopamine levels in striatum homogenates was measured. Tyrosine hydroxylase labeling in the SNc and in the striatum was significantly decreased by 6-OHDA injection, without effect of vitamin A. By contrast, vitamin A supplementation increased striatal expression of D2 and RXR receptors in the striatum of 6-OHDA lesioned rats., Conclusions: Vitamin A supplementation partially alleviates motor alterations and improved striatal function, revealing a possible beneficial preventive approach for PD., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Marie, Leroy, Darricau, Alfos, De Smedt-Peyrusse, Richard, Vancassel and Bosch-Bouju.)
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- 2022
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17. Role of Retinoid X Receptors (RXRs) and dietary vitamin A in Alzheimer's disease: Evidence from clinicopathological and preclinical studies.
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Biyong EF, Tremblay C, Leclerc M, Caron V, Alfos S, Helbling JC, Rodriguez L, Pernet V, Bennett DA, Pallet V, and Calon F
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- Amyloid beta-Peptides metabolism, Amyloid beta-Protein Precursor metabolism, Animals, Diet, Disease Models, Animal, Female, Hippocampus metabolism, Humans, Male, Mice, Mice, Transgenic, Retinoid X Receptors metabolism, tau Proteins metabolism, Alzheimer Disease metabolism, Vitamin A
- Abstract
Background: 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 Aβ
40 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., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2021
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18. Dietary vitamin A supplementation prevents early obesogenic diet-induced microbiota, neuronal and cognitive alterations.
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Biyong EF, Alfos S, Dumetz F, Helbling JC, Aubert A, Brossaud J, Foury A, Moisan MP, Layé S, Richard E, Patterson E, Murphy K, Rea K, Stanton C, Schellekens H, Cryan JF, Capuron L, Pallet V, and Ferreira G
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- Animals, Brain-Gut Axis drug effects, Hippocampus chemistry, Hippocampus drug effects, Male, Memory drug effects, Mice, Mice, Inbred C57BL, Cognition drug effects, Diet, High-Fat adverse effects, Dietary Supplements, Gastrointestinal Microbiome drug effects, Vitamin A administration & dosage, Vitamin A pharmacology
- Abstract
Background: Early consumption of obesogenic diets, rich in saturated fat and added sugar, is associated with a plethora of biological dysfunctions, at both peripheral and brain levels. Obesity is also linked to decreased vitamin A bioavailability, an essential molecule for brain plasticity and memory function., Methods: Here we investigated in mice whether dietary vitamin A supplementation (VAS) could prevent some of the metabolic, microbiota, neuronal and cognitive alterations induced by obesogenic, high-fat and high-sugar diet (HFSD) exposure from weaning to adulthood, i.e. covering periadolescent period., Results: As expected, VAS was effective in enhancing peripheral vitamin A levels as well as hippocampal retinoic acid levels, the active metabolite of vitamin A, regardless of the diet. VAS attenuated HFSD-induced excessive weight gain, without affecting metabolic changes, and prevented alterations of gut microbiota α-diversity. In HFSD-fed mice, VAS prevented recognition memory deficits but had no effect on aversive memory enhancement. Interestingly, VAS alleviated both HFSD-induced higher neuronal activation and lower glucocorticoid receptor phosphorylation in the hippocampus after training., Conclusion: Dietary VAS was protective against the deleterious effects of early obesogenic diet consumption on hippocampal function, possibly through modulation of the gut-brain axis.
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- 2021
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19. Normalization of hippocampal retinoic acid level corrects age-related memory deficits in rats.
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Dumetz F, Buré C, Alfos S, Bonneu M, Richard E, Touyarot K, Marie A, Schmitter JM, Bosch-Bouju C, and Pallet V
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- Animals, Gene Expression drug effects, Rats, Wistar, Tretinoin pharmacology, Tretinoin physiology, Aging, Hippocampus metabolism, Memory, Memory Disorders etiology, Tretinoin metabolism
- Abstract
Dietary micronutrients constitute a major environmental factor influencing aging processes. Vitamin A (vit. A) is the precursor of retinoic acid, a bioactive molecule that controls the expression of several genes involved in brain function. Evidence suggests a reduction of vit. A bioavailability with aging, but its impact on neuronal network is poorly understood. We investigated the mechanisms linking memory impairments with specific alterations of retinoic acid metabolism in the hippocampus. We compared young (10 weeks) and aged (16 months) rats, supplemented or not with dietary vit. A (20 IU retinol/g) for 4 weeks. Our study reveals that aging induced dysregulation of gene expression involved in vit. A and retinoic acid metabolism in the liver. Furthermore, vit. A supplementation restored the integrity of the hippocampal neuronal morphology altered by aging. Importantly, we found a high correlation between hippocampal levels of retinoic acid and memory performance. The present work establishes the link between collapse of retinoid metabolism and age-related cognitive decline, highlighting the role of vit. A in maintaining memory through aging., (Copyright © 2019 Elsevier Inc. All rights reserved.)
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- 2020
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20. Vitamin A deficiency impairs contextual fear memory in rats: Abnormalities in the glucocorticoid pathway.
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Bonhomme D, Alfos S, Webster SP, Wolff M, Pallet V, and Touyarot K
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- Animals, Cognition drug effects, Cognition physiology, Conditioning, Psychological drug effects, Corticosterone blood, Dietary Supplements, Hippocampus drug effects, Hippocampus metabolism, Male, Memory Disorders blood, Rats, Rats, Wistar, Signal Transduction drug effects, Signal Transduction physiology, Spatial Memory drug effects, Spatial Memory physiology, Stress, Psychological, Vitamin A pharmacology, Vitamin A therapeutic use, Vitamin A Deficiency diet therapy, Vitamin A Deficiency pathology, Fear drug effects, Fear psychology, Glucocorticoids metabolism, Memory Disorders etiology, Vitamin A Deficiency complications, Vitamin A Deficiency psychology
- Abstract
Vitamin A and its active metabolite, retinoic acid (RA), play a key role in the maintenance of cognitive functions in the adult brain. Depletion of RA using the vitamin A deficiency (VAD) model in Wistar rats leads to spatial memory deficits in relation to elevated intrahippocampal basal corticosterone (CORT) levels and increased hippocampal 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity. All of these effects are normalised by vitamin A supplementation. However, it is unknown whether vitamin A status also modulates contextual fear conditioning (CFC) in a glucocorticoid-associated fear memory task dependent on the functional integrity of the hippocampus. In the present study, we investigated the impact of VAD and vitamin A supplementation in adult male rats on fear memory processing, plasma CORT levels, hippocampal retinoid receptors and 11β-HSD1 expression following a novelty-induced stress. We also examined whether vitamin A supplementation or a single injection of UE2316, a selective 11β-HSD1 inhibitor, known to modulate local glucocorticoid levels, had any beneficial effects on contextual fear memory and biochemical parameters in VAD rats. We provide evidence that VAD rats exhibit a decreased fear conditioning response during training with a poor contextual fear memory 24 hours later. These VAD-induced cognitive impairments are associated with elevated plasma CORT levels under basal conditions, as well as following a stressful event, with saturated CORT release, altered hippocampal retinoid receptors and 11β-HSD1 expression. Vitamin A supplementation normalises VAD-induced fear conditioning training deficits and all biochemical effects, although it cannot prevent fear memory deficits. Moreover, a single injection of UE2316 not only impairs contextual fear memory, but also reduces plasma CORT levels, regardless of the vitamin A status and decreases slightly hippocampal 11β-HSD1 activity in VAD rats following stress. The present study highlights the importance of vitamin A status with respect to modulating fear memory conditioning in relation to plasma CORT levels and hippocampal 11β-HSD1., (© 2019 British Society for Neuroendocrinology.)
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- 2019
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21. EPA/DHA and Vitamin A Supplementation Improves Spatial Memory and Alleviates the Age-related Decrease in Hippocampal RXRγ and Kinase Expression in Rats.
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Létondor A, Buaud B, Vaysse C, Richard E, Layé S, Pallet V, and Alfos S
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Studies suggest that eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and vitamin A are critical to delay aged-related cognitive decline. These nutrients regulate gene expression in the brain by binding to nuclear receptors such as the retinoid X receptors (RXRs) and the retinoic acid receptors (RARs). Moreover, EPA/DHA and retinoids activate notably kinase signaling pathways such as AKT or MAPK, which includes ERK1/2. This suggests that these nutrients may modulate brain function in a similar way. Therefore, we investigated in middle-aged rats the behavioral and molecular effects of supplementations with EPA/DHA and vitamin A alone or combined. 18-month-old rats exhibited reference and working memory deficits in the Morris water maze, associated with a decrease in serum vitamin A and hippocampal EPA/DHA contents. RARα, RXRβ, and RXRγ mRNA expression and CAMKII, AKT, ERK1/2 expression were decreased in the hippocampus of middle-aged rats. A combined EPA/DHA and vitamin A supplementation had a beneficial additive effect on reference memory but not in working memory in middle-aged rats, associated with an alleviation of the age-related decrease in RXRγ, CAMKII, AKT, and ERK1 expression in the hippocampus. This study provides a new combined nutritional strategy to delay brain aging.
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- 2016
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22. Dietary Polyphenol Supplementation Prevents Alterations of Spatial Navigation in Middle-Aged Mice.
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Bensalem J, Servant L, Alfos S, Gaudout D, Layé S, Pallet V, and Lafenetre P
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Spatial learning and memory deficits associated with hippocampal synaptic plasticity impairments are commonly observed during aging. Besides, the beneficial role of dietary polyphenols has been suggested as potential functional food candidates to prevent this memory decline. Indeed, polyphenols could potentiate the signaling pathways of synaptic plasticity underlying learning and memory. In this study, spatial learning deficits of middle-aged mice were first highlighted and characterized according to their navigation patterns in the Morris water maze task. An eight-week polyphenol-enriched diet, containing a polyphenol-rich extract from grape and blueberry (PEGB; from the Neurophenols Consortium) with high contents of flavonoids, stilbenes and phenolic acids, was then successful in reversing these age-induced effects. The use of spatial strategies was indeed delayed with aging whereas a polyphenol supplementation could promote the occurrence of spatial strategies. These behavioral results were associated with neurobiological changes: while the expression of hippocampal calmodulin kinase II (CaMKII) mRNA levels was reduced in middle-aged animals, the polyphenol-enriched diet could rescue them. Besides, an increased expression of nerve growth neurotrophic factor (NGF) mRNA levels was also observed in supplemented adult and middle-aged mice. Thus these data suggest that supplementation with polyphenols could be an efficient nutritional way to prevent age-induced cognitive decline.
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- 2016
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23. Erythrocyte DHA level as a biomarker of DHA status in specific brain regions of n-3 long-chain PUFA-supplemented aged rats.
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Létondor A, Buaud B, Vaysse C, Fonseca L, Herrouin C, Servat B, Layé S, Pallet V, and Alfos S
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- Aging psychology, Animals, Biomarkers blood, Biomarkers metabolism, Cerebral Cortex metabolism, Corpus Striatum metabolism, Dietary Supplements, Docosahexaenoic Acids metabolism, Erythrocyte Membrane drug effects, Fatty Acids blood, Fatty Acids metabolism, Fatty Acids, Omega-3 administration & dosage, Hippocampus metabolism, Male, Memory physiology, Phosphatidylcholines blood, Phosphatidylcholines metabolism, Phosphatidylethanolamines blood, Phosphatidylethanolamines metabolism, Rats, Rats, Wistar, Aging blood, Aging metabolism, Brain metabolism, Docosahexaenoic Acids blood
- Abstract
n-3 Long-chain PUFA (n-3 LC-PUFA), particularly EPA and DHA, play a key role in the maintenance of brain functions such as learning and memory that are impaired during ageing. Ageing is also associated with changes in the DHA content of brain membranes that could contribute to memory impairment. Limited studies have investigated the effects of ageing and n-3 LC-PUFA supplementation on both blood and brain fatty acid compositions. Therefore, we assessed the relationship between fatty acid contents in plasma and erythrocyte membranes and those in the hippocampus, striatum and cerebral cortex during ageing, and after a 5-month period of EPA/DHA supplementation in rats. In the blood, ageing was associated with an increase in plasma DHA content, whereas the DHA content remained stable in erythrocyte membranes. In the brain, ageing was associated with a decrease in DHA content, which was both region-specific and phospholipid class-specific. In EPA/DHA-supplemented aged rats, DHA contents were increased both in the blood and brain compared with the control rats. The present results demonstrated that n-3 LC-PUFA level in the plasma was not an accurate biomarker of brain DHA status during ageing. Moreover, we highlighted a positive relationship between the DHA levels in erythrocyte phosphatidylethanolamine (PE) and those in the hippocampus and prefrontal cortex in EPA/DHA-supplemented aged rats. Within the framework of preventive dietary supplementation to delay brain ageing, these results suggest the possibility of using erythrocyte PE DHA content as a reliable biomarker of DHA status in specific brain regions.
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- 2014
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24. Vitamin A status regulates glucocorticoid availability in Wistar rats: consequences on cognitive functions and hippocampal neurogenesis?
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Bonhomme D, Minni AM, Alfos S, Roux P, Richard E, Higueret P, Moisan MP, Pallet V, and Touyarot K
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A disruption of the vitamin A signaling pathway has been involved in age-related memory decline and hippocampal plasticity alterations. Using vitamin A deficiency (VAD), a nutritional model leading to a hyposignaling of the retinoid pathway, we have recently demonstrated that retinoic acid (RA), the active metabolite of vitamin A, is efficient to reverse VAD-induced spatial memory deficits and adult hippocampal neurogenesis alterations. Besides, excess of glucocorticoids (GCs) occurring with aging is known to strongly inhibit hippocampal plasticity and functions and few studies report on the counteracting effects of RA signaling pathway on GCs action. Here, we have addressed whether the modulation of brain GCs availability could be one of the biological mechanisms involved in the effects of vitamin A status on hippocampal plasticity and functions. Thus, we have studied the effects of a vitamin A-free diet for 14 weeks and a 4-week vitamin A supplementation on plasma and hippocampal corticosterone (CORT) levels in Wistar rats. We have also investigated corticosteroid binding globulin (CBG) binding capacity and 11beta-Hydrosteroid Dehydrogenase type 1 (11β-HSD1) activity, both important modulators of CORT availability at the peripheral and hippocampal levels respectively. Interestingly, we show that the vitamin A status regulates levels of free plasma CORT and hippocampal CORT levels, by acting through a regulation of CBG binding capacity and 11β-HSD1 activity. Moreover, our results suggest that increased CORT levels in VAD rats could have some deleterious consequences on spatial memory, anxiety-like behavior and adult hippocampal neurogenesis whereas these effects could be corrected by a vitamin A supplementation. Thus, the modulation of GCs availability by vitamin A status is an important biological mechanism that should be taken into account in order to prevent age-related cognitive decline and hippocampal plasticity alterations.
- Published
- 2014
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25. A mid-life vitamin A supplementation prevents age-related spatial memory deficits and hippocampal neurogenesis alterations through CRABP-I.
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Touyarot K, Bonhomme D, Roux P, Alfos S, Lafenêtre P, Richard E, Higueret P, and Pallet V
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- Aging drug effects, Animals, Cell Proliferation, Cell Survival, Dietary Supplements, Hippocampus metabolism, Hippocampus physiopathology, Male, Maze Learning drug effects, Memory, Neurons drug effects, Neurons physiology, Rats, Rats, Wistar, Receptors, Retinoic Acid genetics, Vitamin A pharmacokinetics, Hippocampus drug effects, Memory Disorders prevention & control, Neurogenesis drug effects, Receptors, Retinoic Acid metabolism, Vitamin A administration & dosage
- Abstract
Age-related memory decline including spatial reference memory is considered to begin at middle-age and coincides with reduced adult hippocampal neurogenesis. Moreover, a dysfunction of vitamin A hippocampal signalling pathway has been involved in the appearance of age-related memory deficits but also in adult hippocampal neurogenesis alterations. The present study aims at testing the hypothesis that a mid-life vitamin A supplementation would be a successful strategy to prevent age-related memory deficits. Thus, middle-aged Wistar rats were submitted to a vitamin A enriched diet and were tested 4 months later in a spatial memory task. In order to better understand the potential mechanisms mediating the effects of vitamin A supplementation on hippocampal functions, we studied different aspects of hippocampal adult neurogenesis and evaluated hippocampal CRABP-I expression, known to modulate differentiation processes. Here, we show that vitamin A supplementation from middle-age enhances spatial memory and improves the dendritic arborisation of newborn immature neurons probably resulting in a better survival and neuronal differentiation in aged rats. Moreover, our results suggest that hippocampal CRABP-I expression which controls the intracellular availability of retinoic acid (RA), may be an important regulator of neuronal differentiation processes in the aged hippocampus. Thus, vitamin A supplementation from middle-age could be a good strategy to maintain hippocampal plasticity and functions.
- Published
- 2013
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26. Plasma retinol and association with socio-demographic and dietary characteristics of free-living older persons: the Bordeaux sample of the three-city study.
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Féart C, Siewe A, Samieri C, Peuchant E, Helmer C, Alfos S, Pallet V, and Barberger-Gateau P
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- Aged, Aged, 80 and over, Alcohol Drinking, Animals, Cohort Studies, Cross-Sectional Studies, Demography, Diet Surveys, Female, France, Humans, Income, Male, Marital Status, Meat, Sex Characteristics, Socioeconomic Factors, Surveys and Questionnaires, Vitamin A administration & dosage, Carotenoids administration & dosage, Diet, Vitamin A blood
- Abstract
The objective was to describe retinol plasma concentration and its association with socio-demographic characteristics and dietary habits in French older persons. The study population consisted of 1664 subjects aged 65 + from Bordeaux (France), included in the Three-City cohort. Retinol plasma concentration was determined in fasting blood samples. Dietary assessment was performed by a food frequency questionnaire allowing estimation of weekly intake of dietary sources of vitamin A or provitamin A. The weekly number of glasses of alcohol was also recorded. Age, sex, marital status, educational and income levels, body-mass index (BMI), and smoking were registered. Cross-sectional analysis of the association between plasma retinol and socio-demographic characteristics and dietary habits was performed by multilinear regression. Mean plasma retinol was close to the homeostatically regulated concentration of 2.0 micromol/L but ranged from 0.35 to 6.77 micromol/L. It was higher in women and divorced or separated individuals, and increased with income but not with age or educational level. Plasma retinol was positively and independently associated with the frequency of offal consumption and to the number of glasses of alcohol consumed per week. These results allow targeting older individuals who are at risk of either excessive or deficient vitamin A status and who should benefit from dietary counseling.
- Published
- 2010
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27. T3 administration in adult hypothyroid mice modulates expression of proteins involved in striatal synaptic plasticity and improves motor behavior.
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Vallortigara J, Alfos S, Micheau J, Higueret P, and Enderlin V
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- Age Factors, Animals, Behavior, Animal drug effects, Behavior, Animal physiology, Biomarkers analysis, Biomarkers metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2 drug effects, Calcium-Calmodulin-Dependent Protein Kinase Type 2 metabolism, Corpus Striatum drug effects, Corpus Striatum physiopathology, Disease Models, Animal, Dopamine and cAMP-Regulated Phosphoprotein 32 drug effects, Dopamine and cAMP-Regulated Phosphoprotein 32 metabolism, GTP-Binding Proteins drug effects, GTP-Binding Proteins metabolism, Hypothyroidism complications, Hypothyroidism drug therapy, Male, Methimazole, Mice, Motor Activity physiology, Movement Disorders drug therapy, Movement Disorders etiology, Neurogranin drug effects, Neurogranin metabolism, Phosphorylation drug effects, Presynaptic Terminals drug effects, Presynaptic Terminals metabolism, Propylthiouracil, Receptors, Thyroid Hormone drug effects, Receptors, Thyroid Hormone metabolism, Synaptic Transmission drug effects, Synaptic Transmission physiology, Thyroid Gland drug effects, Thyroid Gland metabolism, Thyroid Gland physiopathology, Up-Regulation drug effects, Up-Regulation physiology, Corpus Striatum metabolism, Hypothyroidism metabolism, Motor Activity drug effects, Movement Disorders metabolism, Neuronal Plasticity drug effects, Triiodothyronine administration & dosage
- Abstract
Adult-onset hypothyroidism is associated with neurological changes such as cognitive dysfunction and impaired learning, which may be related to alterations of synaptic plasticity. We investigate the consequence of adult-onset hypothyroidism on thyroid-mediated transcription events in striatal synaptic plasticity, and the effect of triiodothyronine (T3) replacement. We used hypothyroid mice, treated with propylthiouracil (PTU) and methimazole (MMI), with or without subsequent administration of T3. We evaluated the amount of T3 nuclear receptors (TRalpha1, TRbeta) and striatal plasticity indicators: neurogranin (RC3), Ras homolog enriched in striatum (Rhes), Ca2+/calmodulin-dependent protein kinase (CaMKII), and dopamine- and cAMP-regulated phosphoprotein (DARPP-32). In addition, we assessed hypothyroid mice motor behavior as related to striatum synaptic functions. Hypothyroid mice exhibited significantly reduced TRbeta, RC3 and Rhes expression. T3 administration reversed the expression of TRbeta, RC3, and up-regulated CaMKII levels as well as motor behavior, and decreased DARPP-32 protein phosphorylation. We suggest that thyroid hormone modulation had a major impact on striatal synaptic plasticity of adult mice which produced in turn motor behavior modifications.
- Published
- 2008
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28. Retinoic acid restores adult hippocampal neurogenesis and reverses spatial memory deficit in vitamin A deprived rats.
- Author
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Bonnet E, Touyarot K, Alfos S, Pallet V, Higueret P, and Abrous DN
- Subjects
- Animals, Hippocampus drug effects, Memory Disorders etiology, Rats, Receptor, trkA genetics, Regeneration, Treatment Outcome, Tretinoin pharmacology, Up-Regulation, Vitamin A Deficiency drug therapy, Hippocampus pathology, Memory Disorders drug therapy, Neurogenesis drug effects, Tretinoin therapeutic use, Vitamin A Deficiency complications
- Abstract
A dysfunction of retinoid hippocampal signaling pathway has been involved in the appearance of affective and cognitive disorders. However, the underlying neurobiological mechanisms remain unknown. Hippocampal granule neurons are generated throughout life and are involved in emotion and memory. Here, we investigated the effects of vitamin A deficiency (VAD) on neurogenesis and memory and the ability of retinoic acid (RA) treatment to prevent VAD-induced impairments. Adult retinoid-deficient rats were generated by a vitamin A-free diet from weaning in order to allow a normal development. The effects of VAD and/or RA administration were examined on hippocampal neurogenesis, retinoid target genes such as neurotrophin receptors and spatial reference memory measured in the water maze. Long-term VAD decreased neurogenesis and led to memory deficits. More importantly, these effects were reversed by 4 weeks of RA treatment. These beneficial effects may be in part related to an up-regulation of retinoid-mediated molecular events, such as the expression of the neurotrophin receptor TrkA. We have demonstrated for the first time that the effect of vitamin A deficient diet on the level of hippoccampal neurogenesis is reversible and that RA treatment is important for the maintenance of the hippocampal plasticity and function.
- Published
- 2008
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29. Age-related effects of ethanol consumption on triiodothyronine and retinoic acid nuclear receptors, neurogranin and neuromodulin expression levels in mouse brain.
- Author
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Boucheron C, Alfos S, Enderlin V, Husson M, Pallet V, Jaffard R, and Higueret P
- Subjects
- Age Factors, Analysis of Variance, Animals, Blotting, Western methods, Brain metabolism, Central Nervous System Depressants blood, Ethanol blood, GAP-43 Protein metabolism, Gene Expression physiology, Male, Mice, Mice, Inbred C57BL, Neurogranin genetics, RNA, Messenger metabolism, Receptors, Retinoic Acid genetics, Reverse Transcriptase Polymerase Chain Reaction methods, Triiodothyronine genetics, Triiodothyronine metabolism, Aging, Brain drug effects, Central Nervous System Depressants administration & dosage, Ethanol administration & dosage, Gene Expression drug effects, Neurogranin metabolism, Receptors, Retinoic Acid metabolism
- Abstract
The effects of ethanol consumption and ageing were investigated on the expression levels of retinoic acid (RA) and triiodothyronine (T3) nuclear receptors (RAR, RXR and TR) and of associated target genes involved in synaptic plasticity, neurogranin (RC3) and neuromodulin (GAP-43) in mice brain. For this purpose, C57BL/6 adult and aged mice were subjected to 5-month ethanol consumption and the mRNA expression of RAR, RXR, TR, RC3 and GAP-43 was measured using a real-time RT-PCR method. GAP-43 and RC3 protein levels also were measured by Western blot. Results showed that 12% ethanol consumption in adult mice (11 months) induced an increase in RARbeta, RXRbetagamma and TRalphabeta mRNA level in the brain with only an increase in RC3 expression. The same ethanol consumption in aged mice (22 months) reversed the age-related hypo-expression in brain RARbeta, TRalphabeta and target genes RC3 and GAP-43. Compared with our previous behavioral data showing that ethanol is able to partially suppress a selective age-related cognitive deficit, these results suggest that the ethanol-induced increase in RA and T3 nuclear receptors expression could be one of the mechanisms involved in the normalization of synaptic plasticity-associated gene expression altered in aging brain.
- Published
- 2006
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30. Retinoic acid normalizes nuclear receptor mediated hypo-expression of proteins involved in beta-amyloid deposits in the cerebral cortex of vitamin A deprived rats.
- Author
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Husson M, Enderlin V, Delacourte A, Ghenimi N, Alfos S, Pallet V, and Higueret P
- Subjects
- Amyloid Precursor Protein Secretases, Amyloid beta-Peptides metabolism, Amyloid beta-Protein Precursor metabolism, Animals, Aspartic Acid Endopeptidases, Blotting, Western, Cerebral Cortex metabolism, Cerebral Cortex pathology, Endopeptidases drug effects, Endopeptidases metabolism, Male, Polymerase Chain Reaction, RNA, Messenger analysis, Rats, Rats, Wistar, Receptors, Retinoic Acid metabolism, Vitamin A metabolism, Amyloid beta-Protein Precursor drug effects, Cerebral Cortex drug effects, Receptors, Retinoic Acid drug effects, Tretinoin pharmacology, Vitamin A Deficiency physiopathology
- Abstract
Recent data have revealed that disruption of vitamin A signaling observed in Alzheimer's disease (AD) leads to a deposition of beta-amyloid (Abeta). The aim of this study was to precise the role of vitamin A and its nuclear receptors (RAR) in the processes leading to the Abeta deposits. Thus, the effect of vitamin A depletion and subsequent administration of retinoic acid (RA, the active metabolite of vitamin A) on the expression of RARbeta, and of proteins involved in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the whole brain, hippocampus, striatum, and cerebral cortex of rats. Rats fed a vitamin A-deprived diet for 13 weeks exhibited decreased amount of RARbeta, APP695, BACE, and of APP-CTF in the whole brain and in the cerebral cortex. Administration of RA is able to restore all expression. The results suggest that fine regulation of vitamin A mediated gene expression seems fundamental for the regulation of APP processing.
- Published
- 2006
- Full Text
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31. Triiodothyronine administration reverses vitamin A deficiency-related hypo-expression of retinoic acid and triiodothyronine nuclear receptors and of neurogranin in rat brain.
- Author
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Husson M, Enderlin V, Alfos S, Féart C, Higueret P, and Pallet V
- Subjects
- Animals, Blotting, Western methods, Calmodulin-Binding Proteins genetics, Diterpenes, GTP-Binding Proteins analysis, GTP-Binding Proteins genetics, Liver chemistry, Male, Nerve Tissue Proteins genetics, Neurogranin, Protein Glutamine gamma Glutamyltransferase 2, RNA, Messenger analysis, Rats, Rats, Wistar, Receptors, Retinoic Acid analysis, Receptors, Retinoic Acid genetics, Receptors, Thyroid Hormone genetics, Retinoid X Receptors, Retinyl Esters, Reverse Transcriptase Polymerase Chain Reaction, Transcription Factors analysis, Transcription Factors genetics, Transglutaminases analysis, Transglutaminases genetics, Tretinoin pharmacology, Triiodothyronine blood, Vitamin A analysis, Vitamin A blood, Vitamin A Deficiency drug therapy, Brain Chemistry, Calmodulin-Binding Proteins analysis, Nerve Tissue Proteins analysis, Receptors, Thyroid Hormone analysis, Tretinoin analysis, Triiodothyronine pharmacology, Vitamin A analogs & derivatives, Vitamin A Deficiency metabolism
- Abstract
Recent studies have revealed that retinoids play an important role in the adult central nervous system and cognitive functions. Previous investigations in mice have shown that vitamin A deficiency (VAD) generates a hypo-expression of retinoic acid (RA, the active metabolite of vitamin A) receptors and of neurogranin (RC3, a neuronal protein involved in synaptic plasticity) and a concomitant selective behavioural impairment. Knowing that RC3 is both a triiodothyronine (T3) and a RA target gene, and in consideration of the relationships between the signalling pathways of retinoids and thyroid hormones, the involvement of T3 on RA signalling functionality in VAD was investigated. Thus, the effects of vitamin A depletion and subsequent administration with RA and/or T3 on the expression of RA nuclear receptors (RAR, RXR), T3 nuclear receptor (TR) and on RC3 in the brain were examined. Rats fed a vitamin A-deficient diet for 10 weeks exhibited a decreased expression of RAR, RXR and TR mRNA and of RC3 mRNA and proteins. RA administration to these vitamin A-deficient rats reversed only the RA hypo-signalling in the brain. Interestingly, T3 is able to restore its own brain signalling simultaneously with that of vitamin A and the hypo-expression of RC3. These results obtained in vivo revealed that one of the consequences of VAD is a dysfunction in the thyroid signalling pathway in the brain. This seems of crucial importance since the down regulation of RC3 observed in the depleted rats was corrected only by T3.
- Published
- 2003
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32. A retinoic acid receptor antagonist suppresses brain retinoic acid receptor overexpression and reverses a working memory deficit induced by chronic ethanol consumption in mice.
- Author
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Alfos S, Boucheron C, Pallet V, Higueret D, Enderlin V, Béracochéa D, Jaffard R, and Higueret P
- Subjects
- Animals, Ethanol blood, Male, Memory drug effects, Mice, Mice, Inbred C57BL, Nutritional Physiological Phenomena, Protein Isoforms genetics, RNA, Messenger metabolism, Receptors, Retinoic Acid genetics, Reference Values, Retinoid X Receptors, Time Factors, Transcription Factors genetics, Transglutaminases genetics, Transglutaminases metabolism, Weight Gain, Alcohol Drinking psychology, Brain metabolism, Memory Disorders psychology, Receptors, Retinoic Acid antagonists & inhibitors
- Abstract
Background: Chronic ethanol consumption induces disorders in the biosynthesis of retinoic acid, an active derivative of vitamin A. Recent evidence suggests that an alteration in the retinoic acid signaling pathway leads to impairments in learning and memory in adult mice. We have previously shown that chronic ethanol consumption in mice produces an increased expression of the brain retinoic acid receptor beta (RARbeta) mRNA. These results prompted us to examine whether suppressing the overexpression of retinoid receptors in alcohol-treated mice by RAR antagonist administration would reverse their cognitive impairment., Methods: After 10 months of ethanol consumption (12% v/v in drinking water), C57BL/6 mice were submitted to a working memory task in a T-maze. Then, mice of the control and the ethanol-treated groups received an RARbeta antagonist (CD2665 0.6 mg/kg) for 22 days. The behavioral effect of CD2665 administration was evaluated on a spontaneous alternation task and the neurochemical effect was measured by quantifying the mRNA expression of RARalpha, RARbeta, retinoid X receptor (RXRbeta/gamma) and tissue transglutaminase (tTG; a retinoic acid-target gene)., Results: Mice submitted to ethanol treatment exhibited a progressive decrease in spontaneous alternation rates over successive trials. Moreover, these mice displayed an increased expression of brain RARbeta and RXRbeta/gamma mRNA, together with an increased level of tTG mRNA and enzymatic activity. The administration of CD2665 to alcohol-treated mice totally reversed the working memory deficit and suppressed the overexpression of brain RARbeta, RXRbeta/gamma and tTG mRNA, whereas the same treatment in control mice decreased only the RARbeta mRNA level without affecting memory performance., Conclusion: These data point to the potential role of the retinoid signaling pathway in memory processes and suggest that the overexpression of brain RARbeta and RXRbeta/gamma could be responsible, at least in part, for some memory impairments observed during chronic ethanol consumption.
- Published
- 2001
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33. [In vitro cell cultures in acute leukaemia (author's transl)].
- Author
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Florensa Brichs L, Nomdedeu Tobella B, Gallego Alfos S, Brugues Riera R, Vives Corrons JL, and Rozman C
- Subjects
- Acute Disease, Adolescent, Adult, Aged, Bone Marrow Cells, Cell Division, Cells, Cultured, Colony-Stimulating Factors metabolism, Colony-Stimulating Factors physiology, Female, Hematopoietic Stem Cells metabolism, Humans, Leukemia metabolism, Male, Middle Aged, Prognosis, Hematopoietic Stem Cells growth & development, Leukemia pathology
- Published
- 1981
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