ArticleMolecular psychiatry2012
Functional gene group analysis identifies synaptic gene groups as risk factor for schizophrenia.
Article in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 4 of them syntheses that pooled it.
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Who cites it
101 citing papers in PubMed, 4 syntheses or guidelines pooled it, 171 citations in OpenAlex.
- Evaluating historical candidate genes for schizophrenia.Molecular psychiatry · 2015Pooled it
- Pooled it
- A meta-analysis of gene expression quantitative trait loci in brain.Translational psychiatry · 2014Pooled it
- Multi-locus genome-wide association analysis supports the role of glutamatergic synaptic transmission in the etiology of major depressive disorder.Translational psychiatry · 2012Pooled it
- Mapping topological abnormalities in cortical similarity networks to schizophrenia-associated gene expression.Dialogues in clinical neuroscience · 2026Article
- The expanding roles of adhesion GPCRs in neural circuit assembly.Molecules and cells · 2026Review
- Pathway-Informed Machine Learning Identifies Genetic Predictors of High-Dose Methotrexate-Induced Mucositis in Pediatric Acute Lymphoblastic Leukemia.Clinical pharmacology and therapeutics · 2026Article
- The relationship between schizophrenia polygenic scores, blood-based proteins and psychosis diagnosis in the UK Biobank.Schizophrenia (Heidelberg, Germany) · 2026Article
- Analyses of GWAS and Sub-Threshold Loci Lead to the Discovery of Dendrite Development and Morphology Dysfunction Underlying Schizophrenia Genetic Risk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Isoform-level profiling of mScience advances · 2025Article
- Prioritizing effector genes at trait-associated loci using multimodal evidence.Nature genetics · 2025Article
- Genetic mechanisms for impaired synaptic plasticity in schizophrenia revealed by computational modeling.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Generation and initial characterization of mice lacking full-length BAI3 (ADGRB3) expression.Basic & clinical pharmacology & toxicology · 2023Article
- BioNAR: an integrated biological network analysis package in bioconductor.Bioinformatics advances · 2023Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- WebCSEA: web-based cell-type-specific enrichment analysis of genes.Nucleic acids research · 2022Article
- Modified climbing fiber/Purkinje cell synaptic connectivity in the cerebellum of the neonatal phencyclidine model of schizophrenia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Insights into the Promising Prospect of G Protein and GPCR-Mediated Signaling in Neuropathophysiology and Its Therapeutic Regulation.Oxidative medicine and cellular longevity · 2022Review
- Article
- Microglial-expressed genetic risk variants, cognitive function and brain volume in patients with schizophrenia and healthy controls.Translational psychiatry · 2021Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schizophrenia is a highly heritable disorder with a polygenic pattern of inheritance and a population prevalence of ~1%. Previous studies have implicated synaptic dysfunction in schizophrenia. We tested the accumulated association of genetic variants in expert-curated synaptic gene groups with schizophrenia in 4673 cases and 4965 healthy controls, using functional gene group analysis. Identifying groups of genes with similar cellular function rather than genes in isolation may have clinical implications for finding additional drug targets. We found that a group of 1026 synaptic genes was significantly associated with the risk of schizophrenia (P=7.6 × 10(-11)) and more strongly associated than 100 randomly drawn, matched control groups of genetic variants (P<0.01). Subsequent analysis of synaptic subgroups suggested that the strongest association signals are derived from three synaptic gene groups: intracellular signal transduction (P=2.0 × 10(-4)), excitability (P=9.0 × 10(-4)) and cell adhesion and trans-synaptic signaling (P=2.4 × 10(-3)). These results are consistent with a role of synaptic dysfunction in schizophrenia and imply that impaired intracellular signal transduction in synapses, synaptic excitability and cell adhesion and trans-synaptic signaling play a role in the pathology of schizophrenia.
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