Evidence map›Paper›PMID 27484949›Full record

ArticleScientific reports2016

microRNA-132/212 deficiency enhances Aβ production and senile plaque deposition in Alzheimer's disease triple transgenic mice.

Julia Hernandez-Rapp, Sara Rainone, Claudia Goupil, Véronique Dorval, Pascal Y Smith, Martine Saint-Pierre, Maxime Vallée, Emmanuel Planel, Arnaud Droit, Frédéric Calon and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 5% 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

90 citing papers in PubMed, 2 syntheses or guidelines pooled it, 147 citations in OpenAlex.

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30 more citing papers are in PubMed but not listed here.

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

12 authors at 1 institution in 1 country.

Julia Hernandez-RappAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Sara RainoneAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Claudia GoupilAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Véronique DorvalAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Pascal Y SmithAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Martine Saint-PierreAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Maxime ValléeAxe Endocrinologie et néphrologie, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Emmanuel PlanelAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Arnaud DroitAxe Endocrinologie et néphrologie, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Frédéric CalonAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Francesca CicchettiAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Sébastien S HébertAxe Neurosciences, CHU de Québec-Université Laval, Québec, QC, G1V4G2, Canada.
Université Laval · CA

Funding

CIHR
6 · The paper itself

Abstract

The abnormal regulation of amyloid-β (Aβ) metabolism (e.g., production, cleavage, clearance) plays a central role in Alzheimer's disease (AD). Among endogenous factors believed to participate in AD progression are the small regulatory non-coding microRNAs (miRs). In particular, the miR-132/212 cluster is severely reduced in the AD brain. In previous studies we have shown that miR-132/212 deficiency in mice leads to impaired memory and enhanced Tau pathology as seen in AD patients. Here we demonstrate that the genetic deletion of miR-132/212 promotes Aβ production and amyloid (senile) plaque formation in triple transgenic AD (3xTg-AD) mice. Using RNA-Seq and bioinformatics, we identified genes of the miR-132/212 network with documented roles in the regulation of Aβ metabolism, including Tau, Mapk, and Sirt1. Consistent with these findings, we show that the modulation of miR-132, or its target Sirt1, can directly regulate Aβ production in cells. Finally, both miR-132 and Sirt1 levels correlated with Aβ load in humans. Overall, our results support the hypothesis that the miR-132/212 network, including Sirt1 and likely other target genes, contributes to abnormal Aβ metabolism and senile plaque deposition in AD. This study strengthens the importance of miR-dependent networks in neurodegenerative disorders, and opens the door to multifactorial drug targets of AD by targeting Aβ and Tau.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimalHumansMiceMice, TransgenicMicroRNAsSirtuin 1Amyloid beta-PeptidesMicroRNAsMIRN132 microRNA, mouseMIRN212 microRNA, mouseSirt1 protein, mouseSirtuin 1

Identifiers

PMID27484949
PMCPMC4971468
OpenAlexW2475682196

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.