Evidence map›Paper›PMID 29442441›Full record

ReviewAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2018

A comprehensive review of the genetic and biological evidence supports a role for MicroRNA-137 in the etiology of schizophrenia.

Kensuke Sakamoto, James J Crowley

Abstract readReview
In one paragraph

Review in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  13. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. MicroRNA137-loaded lipid nanoparticles regulate synaptic proteins in the prefrontal cortex.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  15. Article
  16. Review
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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

2 authors at 1 institution in 2 countries.

Kensuke SakamotoDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.ORCID 0000-0003-4488-1244
James J CrowleyDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
University of North Carolina at Chapel Hill · US

Funding

Genetic & Environmental Predictors of Tourette Syndrome & OCD in DenmarkR01MH105500 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CROWLEY, JAMES JOSEPH · 2015 to 2019
$3.0M
OCD: Novel Comparative Genomic Approaches to Identify Disease and Treatment MechanismsR01MH110427 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CROWLEY, JAMES JOSEPH · 2016 to 2021
$3.0M
The MIR137 region in schizophrenia: genomics, variant discovery & associationR21MH099370 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SULLIVAN, PATRICK F, SZATKIEWICZ, JIN PENG · 2013 to 2014
$418k
The schizophrenia candidate gene MIR137: functional studies in mouseR21MH102814 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SAKAMOTO, KENSUKE, SULLIVAN, PATRICK F · 2014 to 2015
$418k
NIMH NIH HHS R01 MH105500NIMH NIH HHS R01 MH110427NIMH NIH HHS R21 MH099370NIMH NIH HHS R21 MH102814
6 · The paper itself

Abstract

Since it was first associated with schizophrenia (SCZ) in a 2011 genome-wide association study (GWAS), there have been over 100 publications focused on MIR137, the gene encoding microRNA-137. These studies have examined everything from its fundamental role in the development of mice, flies, and fish to the intriguing enrichment of its target gene network in SCZ. Indeed, much of the excitement surrounding MIR137 is due to the distinct possibility that it could regulate a gene network involved in SCZ etiology, a disease which we now recognize is highly polygenic. Here we comprehensively review, to the best of our ability, all published genetic and biological evidence that could support or refute a role for MIR137 in the etiology of SCZ. Through a careful consideration of the literature, we conclude that the data gathered to date continues to strongly support the involvement of MIR137 and its target gene network in neuropsychiatric traits, including SCZ risk. There remain, however, more unanswered than answered questions regarding the mechanisms linking MIR137 genetic variation with behavior. These questions need answers before we can determine whether there are opportunities for diagnostic or therapeutic interventions based on MIR137. We conclude with a number of suggestions for future research on MIR137 that could help to provide answers and hope for a greater understanding of this devastating disorder.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyHumansMicroRNAsMultifactorial InheritancePhenotypePolymorphism, Single NucleotideRisk FactorsSchizophreniaMicroRNAsMIRN137 microRNA, humanGWASmicroRNAmiR-137schizophreniaSNP

Identifiers

PMID29442441
PMCPMC5815396
OpenAlexW2624881536

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.