Evidence map›Paper›PMID 34737043›Full record

ArticleNeurobiology of disease2021

Role of Retinoid X Receptors (RXRs) and dietary vitamin A in Alzheimer's disease: Evidence from clinicopathological and preclinical studies.

Essi F Biyong, Cyntia Tremblay, Manon Leclerc, Vicky Caron, Serge Alfos, Jean-Christophe Helbling, Léa Rodriguez, Vincent Pernet, David A Bennett, Véronique Pallet and 1 more

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 3 countries.

Essi F BiyongUniv. Bordeaux, INRAE, Bordeaux INP, NutriNeuro, UMR 1286, F-33000 Bordeaux, France; Faculté de pharmacie, Université Laval, Québec, Québec, Canada; Centre de recherche du CHU de Québec-Université Laval (CHUL), Axe Neurosciences, 2705 Boulevard Laurier, Québec, Québec, Canada; Institut sur la Nutrition et les Aliments Fonctionnels (INAF), Québec, Québec, Canada; LIA OptiNutriBrain - Laboratoire International Associé (NutriNeuro France-INAF Canada), Canada.
Cyntia TremblayFaculté de pharmacie, Université Laval, Québec, Québec, Canada; Centre de recherche du CHU de Québec-Université Laval (CHUL), Axe Neurosciences, 2705 Boulevard Laurier, Québec, Québec, Canada.
Manon LeclercFaculté de pharmacie, Université Laval, Québec, Québec, Canada; Centre de recherche du CHU de Québec-Université Laval (CHUL), Axe Neurosciences, 2705 Boulevard Laurier, Québec, Québec, Canada.
Vicky CaronFaculté de pharmacie, Université Laval, Québec, Québec, Canada; Centre de recherche du CHU de Québec-Université Laval (CHUL), Axe Neurosciences, 2705 Boulevard Laurier, Québec, Québec, Canada.
Serge AlfosUniv. Bordeaux, INRAE, Bordeaux INP, NutriNeuro, UMR 1286, F-33000 Bordeaux, France.
Jean-Christophe HelblingUniv. Bordeaux, INRAE, Bordeaux INP, NutriNeuro, UMR 1286, F-33000 Bordeaux, France.
Léa RodriguezCUO-Recherche, Centre de Recherche du CHU de Québec, Québec, QC, Canada; Département d'ophtalmologie, Faculté de Médecine, Université Laval, Québec, QC, Canada.
Vincent PernetCUO-Recherche, Centre de Recherche du CHU de Québec, Québec, QC, Canada; Département d'ophtalmologie, Faculté de Médecine, Université Laval, Québec, QC, Canada.
David A BennettRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
Véronique PalletUniv. Bordeaux, INRAE, Bordeaux INP, NutriNeuro, UMR 1286, F-33000 Bordeaux, France; LIA OptiNutriBrain - Laboratoire International Associé (NutriNeuro France-INAF Canada), Canada.
Frédéric CalonFaculté de pharmacie, Université Laval, Québec, Québec, Canada; Centre de recherche du CHU de Québec-Université Laval (CHUL), Axe Neurosciences, 2705 Boulevard Laurier, Québec, Québec, Canada; Institut sur la Nutrition et les Aliments Fonctionnels (INAF), Québec, Québec, Canada; LIA OptiNutriBrain - Laboratoire International Associé (NutriNeuro France-INAF Canada), Canada. Electronic address: frederic.calon@crchudequebec.ulaval.ca.
Université Laval · CACentre hospitalier de l'Université Laval · CAInstitut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement · FRInstitut Polytechnique de Bordeaux · FRNutriNeuro · FRRush University Medical Center · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI LEURGANS, SUE E. · 1991 to 2020
$49.1M
Risk Factors, Pathology, and Clinical Expressions of ADRF1AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2014 to 2014
$6.0M
NIA NIH HHS P30 AG010161NIA NIH HHS RF1 AG015819
6 · The paper itself

Abstract

backgroundVitamin 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.

methodsWe 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).

resultsThe 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

conclusionOur 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.

Indexed as

Alzheimer DiseaseVitamin AAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDietDisease Models, AnimalFemaleHippocampusHumansMaleMiceMice, TransgenicRetinoid X Receptorstau ProteinsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorRetinoid X Receptorstau ProteinsVitamin A3xTg-AD mouseAgingAlzheimer's diseaseAmyloidDietPreventionRXRsSexVitamin A

Identifiers

PMID34737043
PMCPMC8649044
OpenAlexW3210621912

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.