Genome-wide association study identifies five new schizophrenia loci
Open accessAbstract
We examined the role of common genetic variation in schizophrenia in a genome-wide association study of substantial size: a stage 1 discovery sample of 21,856 individuals of European ancestry and a stage 2 replication sample of 29,839 independent subjects. The combined stage 1 and 2 analysis yielded genome-wide significant associations with schizophrenia for seven loci, five of which are new (1p21.3, 2q32.3, 8p23.2, 8q21.3 and 10q24.32-q24.33) and two of which have been previously implicated (6p21.32-p22.1 and 18q21.2). The strongest new finding (P = 1.6 × 10(-11)) was with rs1625579 within an intron of a putative primary transcript for MIR137 (microRNA 137), a known regulator of neuronal development. Four other schizophrenia loci achieving genome-wide significance contain predicted targets of MIR137, suggesting MIR137-mediated dysregulation as a previously unknown etiologic mechanism in schizophrenia. In a joint analysis with a bipolar disorder sample (16,374 affected individuals and 14,044 controls), three loci reached genome-wide significance: CACNA1C (rs4765905, P = 7.0 × 10(-9)), ANK3 (rs10994359, P = 2.5 × 10(-8)) and the ITIH3-ITIH4 region (rs2239547, P = 7.8 × 10(-9)).
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miR-137 regulates neurodevelopment and synaptic signaling genes, such as CACNA1C and TCF4.
“This miRNA regulates neurodevelopment and synaptic signaling genes, such as CACNA1C and TCF4”
From The clinical use of epigenetics in psychiatry: a narrative review of epigenetic mechanisms, key candidate genes, and precision psychiatry (2025) · cites this paper as [32]
The paper’s MIR137 discussion (section labeled Abstract; page unavailable) implicates it in adult neurogenesis and neuronal maturation and identifies both CACNA1C and TCF4 as predicted targets. It reports evidence that MIR137 changes TCF4 protein expression, but does not establish regulation of CACNA1C or describe these targets as synaptic-signaling genes. (LLM, conf=0.85)
Experimental — accuracy not yet measuredmiR-137 is one of the most significant risk loci for schizophrenia from GWAS.
“Genome-wide association studies (GWAS) in schizophrenia have implicated miR-137 as one of the most significant risk loci for schizophrenia”
From The clinical use of epigenetics in psychiatry: a narrative review of epigenetic mechanisms, key candidate genes, and precision psychiatry (2025) · cites this paper as [32]
In a gene-based analysis using meta-analytic p values from the largest schizophrenia GWAS (9,394 cases and 12,462 controls), 8 out of 36 tested autosomal genes of the CYFIP1 interactome had a nominally significant p value (<0.05) for association with schizophrenia.
“a gene-based analysis interrogating for association with schizophrenia based on the meta-analytic p values obtained by the largest schizophrenia genome-wide association study to date (Ripke et al., 2011) (9,394 cases and 12,462 controls) revealed that 8 out of 36 tested autosomal genes of the CYFIP1 interactome had a nominally significant p value (<0.05) for association with schizophrenia (Tables”
From CYFIP1 Coordinates mRNA Translation and Cytoskeleton Remodeling to Ensure Proper Dendritic Spine Formation (2013) · cites this paper as Ripke et al., 2011
Large-scale studies are underway through international efforts including the Psychiatric Genomics Consortium and the Wellcome Trust Case Control Consortium.
“Such large scale studies are underway through International efforts including by the Psychiatric Genomics Consortium (PGC) (Ripke et al., 2011) and Wellcome Trust Case Control Consortium (WTCCC).”
From CNVs: Harbingers of a Rare Variant Revolution in Psychiatric Genetics (2012) · cites this paper as Ripke et al., 2011
Large-scale meta-analysis of GWAS has obtained statistically convincing evidence for common variants in schizophrenia and bipolar disorder.
“Large Scale meta-analysis of GWAS has obtained statistically convincing evidence for common variants in schizophrenia (Ripke et al., 2011) and bipolar disorder (Sklar et al., 2011).”
From CNVs: Harbingers of a Rare Variant Revolution in Psychiatric Genetics (2012) · cites this paper as Ripke et al., 2011
Microdeletions of miR137 have been reported in ASD, ID, and schizophrenia.
“Microdeletions of miR137 have been reported in ASD,39 ID,40 and schizophrenia.41”
From Convergence of genes and cellular pathways dysregulated in autism spectrum disorders (2014) · cites this paper as [41]
Predicted targets of microRNA-137 were significantly enriched for dURVs (OR=1.13; 95% CI=1.09-1.18; P=6.8e-4).
“Predicted targets of microRNA-13736, previously identified as localized near common SNPs associated with schizophrenia37, were also significantly enriched for dURVs (OR=1.13; 95% CI=1.09–1.18; P = 6.8 × 10−4) (Fig. 2).”
From Increased burden of ultra-rare protein-altering variants among 4,877 individuals with schizophrenia (2016) · cites this paper as [37]
Use of a larger sample size to develop the predictor should produce a more accurate allele score and thus increase the amount of variance in Stage 2 case and control status explained.
“In addition, as pointed out by Ripke et al. (37), the use of a larger sample size to develop the predictor (i.e. model from the Stage 1 sample) should produce a more accurate allele score and thus increase the amount of variance in the Stage 2 case and control status explained.”
From Individual common variants exert weak effects on the risk for autism spectrum disorders (2012) · cites this paper as [37]
Genome-wide association studies show that some proteases involved in ECM remodeling, such as MMP16, are encoded by genes strongly associated with SZ.
“In addition, genome-wide association studies show that some of the proteases involved in ECM remodeling, such as MMP16, are encoded by genes strongly associated with SZ.81”
From Aggrecan and chondroitin-6-sulfate abnormalities in schizophrenia and bipolar disorder: a postmortem study on the amygdala (2015) · cites this paper as [81]
The PGC schizophrenia GWAS yielded 5 genome-wide significant loci and 183 non-GWS loci at P < 10−4; in a follow-up study, 20 of these markers were elevated beyond genome-wide significance.
“A PGC schizophrenia GWAS [40], which was of comparable size to this, yielded 5 GWS loci and 183 non-GWS loci at P < 10−4. In a follow-up study [19], 20 of these markers were elevated beyond GWS; these were not limited to the most highly ranked markers, as the newly GWS markers ranged from 7 to 188 in the original study.”
In the schizophrenia PGC1 study, over 10% (20 of 183 independent loci) of association signals with 5 × 10−8 ≤ P < 10−4 were subsequently reported as genome-wide significant in the schizophrenia PGC2 analysis.
“Previously, when comparing the results of an early iteration of the PGC schizophrenia GWAS (PGC1) [40], which is of similar size to that of reported here for the PGC ASD GWAS, to more recent and larger PGC schizophrenia GWAS (PGC2) [19], we noted that of the association signals 5 × 10−8 ≤ P < 10−4 in the schizophrenia PGC1 study, over 10% (20 of 183 independent loci) were subsequently reported as”
For SCZ and BIP, sign tests comparing the consistency of association tests from discovery GWAS and replication samples for sets of top signals are usually highly significant even if most loci do not meet genome-wide significance.
“For SCZ and BIP, sign tests comparing the consistency of association tests from discovery GWAS and replication samples for sets of top signals are usually highly significant even if most loci do not meet genome-wide significance. 58,59,174”
From Genetic architectures of psychiatric disorders: the emerging picture and its implications (2012) · cites this paper as [59]
A sign test between the discovery and follow-up results was highly significant, again suggesting insufficient power.
“Similarly, a sign test between the discovery and follow-up results was highly significant, again suggesting insufficient power. 59”
From Genetic architectures of psychiatric disorders: the emerging picture and its implications (2012) · cites this paper as [59]
For BIP, the discovery phase consisted of 7,481 cases and 9,250 controls with follow-up of 34 statistically independent loci in around 4,500 cases. Two loci exceeded genome-wide significance.
“For BIP, the discovery phase consisted of 7,481 cases and 9,250 controls with follow-up of 34 statistically independent loci in around 4,500 cases. Two loci exceeded genome-wide significance (Table 3).”
From Genetic architectures of psychiatric disorders: the emerging picture and its implications (2012) · cites this paper as [59]
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- Authors
- The Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium
- Venue
- Nature Genetics
- Published
- 2011-09-18
- Volume
- 43
- Issue
- 10
- Pages
- 969-976
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3303194
- OpenAlex
- W2161527093
- Cited by
- 1,919
- References
- 32
- Citations by year
- 2026: 23 · 2025: 48 · 2024: 63 · 2023: 60 · 2022: 100 · 2021: 100 · 2020: 103 · 2019: 113 · 2018: 119 · 2017: 140 · 2016: 170 · 2015: 202 · 2014: 235 · 2013: 230 · 2012: 194
- FWCI
- 148.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (publishedVersion, other-oa)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, other-oa)
- VU Research Portal (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Publications (Maastricht University) (submittedVersion, cc-by-nc-sa)
- QUT ePrints (Queensland University of Technology) (submittedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Arrow@dit (Dublin Institute of Technology) (submittedVersion, cc-by-nc-sa)
- UCL Discovery (University College London) (submittedVersion)
- JuSER (Forschungszentrum Jülich) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Lirias (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- Explore Bristol Research (submittedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (submittedVersion)
- Hirsla (Landspítali University Hospital) (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- Lenus, The Irish Health Repository (Dr Steevens Hospital Library) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- Research Publications (Maastricht University) (submittedVersion)
- Faculty of Health; Institute of Health and Biomedical Innovation
- Funders
- U.S. Department of Veterans Affairs
- Massachusetts General Hospital
- University of Southern California
- Emory University
- Yeshiva University
- Aarhus Universitet
- Aarhus Universitetshospital
- Helsingin Yliopisto
- Johns Hopkins University
- Georgetown University
- Louisiana State University
- Virginia Commonwealth University
- London School of Hygiene and Tropical Medicine
- Northern California Institute for Research and Education
- Wellcome Trust (WTCCC2, 090532)
- NorthShore University HealthSystem
- Broad Institute
- King's College London
- University College London
- University of Oxford
- Cardiff University
- University of Aberdeen
- Hunter Medical Research Institute
- Trinity College Dublin
- Universität Heidelberg
- Institut National de la Santé et de la Recherche Médicale
- Rijksuniversiteit Groningen
- University of New South Wales
- University of Melbourne
- Universiteit van Amsterdam
- Universiteit Maastricht
- Semmelweis Egyetem
- Gentofte Hospital
- Hebrew University of Jerusalem
- University of Toronto
- Karolinska Institutet
- Centre National de la Recherche Scientifique
- Universitair Medisch Centrum Groningen
- National and Kapodistrian University of Athens
- Universitetet i Oslo
- Háskóli Íslands
- Università degli Studi di Verona
- Diakonhjemmet
- Rheinische Friedrich-Wilhelms-Universität Bonn
- Terveyden ja hyvinvoinnin laitos
- National Institutes of Health
- Albert Einstein College of Medicine, Yeshiva University
- University of North Carolina at Chapel Hill
- Johns Hopkins Bloomberg School of Public Health
- University of Colorado Denver
- Department of Psychiatry, Columbia University
- Department of Psychiatry, University of Toronto
- Roy J. and Lucille A. Carver College of Medicine, University of Iowa
- School of Medicine, Virginia Commonwealth University
- Medical Research Council
- Menzies Centre for Australian Studies, King's College London, University of London
- Queensland Brain Institute
- Diamantina Institute, University of Queensland
- National Heart, Lung, and Blood Institute
- National Institute of Mental Health (K23MH001760, R01MH062276, R01MH077139, U01MH085518, P30MH074543, P50MH066392, R01MH061884, U01MH085520, R01MH059566, R01MH058693, R01MH060879, R01MH060870, U01MH094421, K01MH085812, R01MH061675, R01MH078075, R01MH085548, R01MH059586, R01MH071681, R01MH083094, R01MH059588, R01MH067257, U01MH079470, R01MH074027, U01MH085515, R01MH068881, R01MH079800, R01MH084098, R01MH059587, R01MH068921, R01MH080403)
- National Cancer Institute (R01CA082659, P01CA142538)
- National Institute of General Medical Sciences (T32GM007753, R37GM047845)
- Division of Cancer Epidemiology and Genetics, National Cancer Institute
- 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 › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Keywords
- schizophrenia, genetic loci, microRNA-137, CACNA1C, ANK3, bipolar disorder, neuronal development, intronic variants, schizophrenia risk genes
- MeSH terms
- Alleles, Bipolar Disorder, Female, Gene Expression Regulation, Haplotypes, Humans, Male, Mutation, Schizophrenia, Linkage Disequilibrium, Genome, Human, Logistic Models, Case-Control Studies, Gene Dosage, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, MicroRNAs, White People, Genome-Wide Association Study, Genetic Loci
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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