Evidence map›Paper›PMID 22733126›Full record

ArticleMolecular psychiatry2013

Genome-wide supported variant MIR137 and severe negative symptoms predict membership of an impaired cognitive subtype of schizophrenia.

M J Green, M J Cairns, J Wu, M Dragovic, A Jablensky, P A Tooney, R J Scott, V J Carr, Australian Schizophrenia Research Bank

Erratum issuedAbstract read
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In one paragraph

Article in Molecular psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 87 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 5 pooled it
11.2field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 5 syntheses or guidelines pooled it, 151 citations in OpenAlex.

  1. Pooled it
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  6. Article
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  11. Cognitive subtypes in youth at clinical high risk for psychosis.Psychiatry and clinical neurosciences · 2025
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  16. Transdiagnostic subgroups of cognitive impairment in early affective and psychotic illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  17. Article
  18. Genetic and Epigenetic Regulation inInternational journal of molecular sciences · 2023
    Article
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  20. Review

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

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

M J GreenSchool of Psychiatry, University of New South Wales, Research Unit for Schizophrenia Epidemiology, St Vincent's Hospital, Darlinghurst, NSW, Australia. melissa.green@unsw.edu.au
M J Cairns
J Wu
M Dragovic
A Jablensky
P A Tooney
R J Scott
V J Carr
Australian Schizophrenia Research Bank
University of Newcastle Australia · AUUniversity of Western Australia · AUUNSW Sydney · AUJohn Hunter Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progress in determining the aetiology of schizophrenia (Sz) has arguably been limited by a poorly defined phenotype. We sought to delineate empirically derived cognitive subtypes of Sz to investigate the association of a genetic variant identified in a recent genome-wide association study with specific phenotypic characteristics of Sz. We applied Grade of Membership (GoM) analyses to 617 patients meeting ICD-10 criteria for Sz (n=526) or schizoaffective disorder (n=91), using cognitive performance indicators collected within the Australian Schizophrenia Research Bank. Cognitive variables included subscales from the Repeatable Battery for the Assessment of Neuropsychological Status, the Controlled Oral Word Association Test and the Letter Number Sequencing Test, and standardised estimates of premorbid and current intelligence quotient. The most parsimonious GoM solution yielded two subtypes of clinical cases reflecting those with cognitive deficits (CDs; N=294), comprising 47.6% of the sample who were impaired across all cognitive measures, and a cognitively spared group (CS; N=323) made up of the remaining 52.4% who performed relatively well on all cognitive tests. The CD subgroup were more likely to be unemployed, had an earlier illness onset, and greater severity of functional disability and negative symptoms than the CS group. Risk alleles on the MIR137 single-nucleotide polymorphism (SNP) predicted membership of CD subtype only in combination with higher severity of negative symptoms. These findings provide the first evidence for association of the MIR137 SNP with a specific Sz phenotype characterised by severe CDs and negative symptoms, consistent with the emerging role of microRNAs in the regulation of proteins responsible for neural development and function.

Indexed as

Genome-Wide Association StudySchizophrenic PsychologyAdultAllelesCase-Control StudiesCognition DisordersFemaleGenetic Predisposition to DiseaseHumansIntelligence TestsMaleMicroRNAsNeuropsychological TestsPolymorphism, Single NucleotidePsychotic DisordersSchizophreniaMicroRNAs

Identifiers

PMID22733126
OpenAlexW2015534638

What OpenQuestion holds

Textmetadata
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.