Specific Glial Functions Contribute to Schizophrenia Susceptibility
Open accessAbstract
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.
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Glial/CSPG cluster abnormalities may represent a contributing factor to dysregulated glutamatergic transmission, and more broadly to neuron/glia interactions, in major psychoses.
“Glial/CSPG cluster abnormalities may thus represent a contributing factor to dysregulated glutamatergic transmission, and more broadly to neuron/glia interactions, in major psychoses.15, 22, 105, 106”
From Aggrecan and chondroitin-6-sulfate abnormalities in schizophrenia and bipolar disorder: a postmortem study on the amygdala (2015) · cites this paper as [105]
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- Authors
- Goudriaan, A., de Leeuw, C., Ripke, S., Hultman, C. M., Sklar, P., Sullivan, P. F., Smit, A. B., Posthuma, D., & Verheijen, M. H. G.
- Affiliations
- Amsterdam Neuroscience (NL)
- Broad Institute (US)
- Karolinska Institutet (SE)
- Icahn School of Medicine at Mount Sinai (US)
- University of North Carolina at Chapel Hill (US)
- Venue
- Schizophrenia Bulletin
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-08-16
- Volume
- 40
- Issue
- 4
- Pages
- 925-935
- ISSN
- 0586-7614 (ISSN-L)
- 1745-1701
- PMC
- PMC4059439
- OpenAlex
- W2102430481
- Cited by
- 114
- References
- 73
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 8 · 2023: 4 · 2022: 8 · 2021: 10 · 2020: 7 · 2019: 6 · 2018: 11 · 2017: 10 · 2016: 12 · 2015: 15 · 2014: 14
- FWCI
- 9.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Schizophrenia Bulletin (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- VU Research Portal (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- UNC Libraries
- Funders
- European Commission (242167)
- Koninklijke Nederlandse Akademie van Wetenschappen
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (NWO 480‐05‐003, 480- 05-003, 645-000-003)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- schizophrenia, glial cells
- MeSH terms
- Astrocytes, Humans, Neuroglia, Oligodendroglia, Schizophrenia, Case-Control Studies, Microglia, Genetic Predisposition to Disease, Genome-Wide Association Study
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