Evidence map›Paper›PMID 23956119›Full record

ArticleSchizophrenia bulletin2014

Specific glial functions contribute to schizophrenia susceptibility.

Andrea Goudriaan, Christiaan de Leeuw, Stephan Ripke, Christina M Hultman, Pamela Sklar, Patrick F Sullivan, August B Smit, Danielle Posthuma, Mark H G Verheijen

Abstract read
In one paragraph

Article in Schizophrenia bulletin, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
–field-weighted citation impact
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

64 citing papers in PubMed.

  1. Article
  2. IncreasingBiological psychiatry global open science · 2025
    Article
  3. Cortical myelin mapping in antipsychotic medication-naïve, first-episode psychosis patients.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  4. Review
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  7. Review
  8. Review
  9. Article
  10. Article
  11. The role of microglia in neuropsychiatric disorders and suicide.European archives of psychiatry and clinical neuroscience · 2022
    Review
  12. Review
  13. Review
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  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

4 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

9 authors.

Andrea GoudriaanDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, the Netherlands; danielle.posthuma@vu.nl.
Christiaan de LeeuwDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, the Netherlands; Institute for Computing and Information Sciences, Radboud University, Nijmegen, the Netherlands;
Stephan RipkeAnalytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA;
Christina M HultmanDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden;
Pamela SklarDepartment of Psychiatry, Mount Sinai School of Medicine, New York, NY;
Patrick F SullivanDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center for Psychiatric Genomics, Department of Genetics, University of North Carolina, Chapel Hill, NC;
August B SmitDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, the Netherlands;
Danielle PosthumaDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, the Netherlands; danielle.posthuma@vu.nl.
Mark H G VerheijenDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, the Netherlands;

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is a highly polygenic brain disorder. The main hypothesis for disease etiology in schizophrenia primarily focuses on the role of dysfunctional synaptic transmission. Previous studies have therefore directed their investigations toward the role of neuronal dysfunction. However, recent studies have shown that apart from neurons, glial cells also play a major role in synaptic transmission. Therefore, we investigated the potential causal involvement of the 3 principle glial cell lineages in risk to schizophrenia. We performed a functional gene set analysis to test for the combined effects of genetic variants in glial type-specific genes for association with schizophrenia. We used genome-wide association data from the largest schizophrenia sample to date, including 13 689 cases and 18 226 healthy controls. Our results show that astrocyte and oligodendrocyte gene sets, but not microglia gene sets, are associated with an increased risk for schizophrenia. The astrocyte and oligodendrocyte findings are related to astrocyte signaling at the synapse, myelin membrane integrity, glial development, and epigenetic control. Together, these results show that genetic alterations underlying specific glial cell type functions increase susceptibility to schizophrenia and provide evidence that the neuronal hypothesis of schizophrenia should be extended to include the role of glia.

Indexed as

AstrocytesCase-Control StudiesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMicrogliaNeurogliaOligodendrogliaSchizophreniagene set analysisgenome-wide associationgliaGWASPGCpsychiatric disease

Identifiers

PMID23956119
PMCPMC4059439

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.