Evidence map›Paper›PMID 25024332›Full record

ArticleJournal of Alzheimer's disease : JAD2014

Upregulation of miR-181 decreases c-Fos and SIRT-1 in the hippocampus of 3xTg-AD mice.

Carlos J Rodriguez-Ortiz, David Baglietto-Vargas, Hilda Martinez-Coria, Frank M LaFerla, Masashi Kitazawa

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

54 citing papers in PubMed, 92 citations in OpenAlex.

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  13. The role of miRNAs in Behçet's disease.Frontiers in immunology · 2023
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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

5 authors at 2 institutions in 1 country.

Carlos J Rodriguez-OrtizSchool of Natural Sciences, University of California, Merced, CA, USA.
David Baglietto-VargasDepartment of Neurobiology and Behavior, University of California, Irvine, CA, USA Institute for Memory Impairments and Neurological Diseases, University of California, Irvine, CA, USA.
Hilda Martinez-CoriaDepartment of Neurobiology and Behavior, University of California, Irvine, CA, USA Institute for Memory Impairments and Neurological Diseases, University of California, Irvine, CA, USA.
Frank M LaFerlaDepartment of Neurobiology and Behavior, University of California, Irvine, CA, USA Institute for Memory Impairments and Neurological Diseases, University of California, Irvine, CA, USA.
Masashi KitazawaSchool of Natural Sciences, University of California, Merced, CA, USA.
University of California, Irvine · USUniversity of California, Merced · US

Funding

Learning and Memory Impairments in Transgenic AD ModelsR01AG027544 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2007 to 2016
$3.1M
NIA NIH HHS 2R01AG027544-06NIA NIH HHS R01 AG027544
6 · The paper itself

Abstract

MicroRNAs are a group of small RNAs that regulate diverse cellular processes including neuronal function. Recent studies have shown that dysregulation of specific microRNAs is critically involved in the development of Alzheimer's disease (AD). Most of these reports have focused on microRNAs implicated in alterations of amyloid-β and tau. However, studies exploring the relation between microRNAs dysregulation in AD and synaptic plasticity are scarce despite the well-known involvement of microRNAs in synaptic plasticity. Since impairments in synaptic plasticity and neuronal loss are two important features displayed in AD patients, it is feasible to hypothesize that alterations in plasticity-related microRNAs underlie AD progression. Here, levels of a small number of microRNAs implicated in normal neuronal function and/or plasticity were examined in an AD model. Twelve-month old 3xTg-AD mice with plaques and tangles presented a significant upregulation of miR-181 in the hippocampus compared to age-matched wild type mice. Increased miR-181 was not detected in pre-pathological 3xTg-AD mice. Analysis of predicted targets of miR-181 identified c-Fos and SIRT-1, proteins critically involved in memory formation. Both c-Fos and SIRT-1 levels were significantly decreased in the ventral hippocampus of twelve-month old 3xTg-AD mice. Overexpression of miR-181 in SH-SY5Y cells significantly decreased c-Fos and SIRT-1, strongly suggesting that miR-181 directly regulates the expression of these two proteins. These findings indicate a connection between miR-181 and proteins involve in synaptic plasticity and memory processing in a transgenic mouse model of AD. Our results suggest that microRNAs involved in synaptic plasticity might be an important factor that contributes to AD neuropathology.

Indexed as

AgingAlzheimer DiseaseAnimalsCell Line, TumorDisease Models, AnimalFemaleHumansMice, TransgenicMicroRNAsProto-Oncogene Proteins c-fosRNA, MessengerSirtuin 1Up-RegulationMicroRNAsmirn181 microRNA, mouseProto-Oncogene Proteins c-fosRNA, MessengerSIRT1 protein, humanSirt1 protein, mouseSirtuin 1Alzheimer's diseasemiRNAsirtuin-1synaptic plasticitytranslational regulation

Identifiers

PMID25024332
PMCPMC7294908
OpenAlexW1555289101

What OpenQuestion holds

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Registered trials

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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.