ArticleNature neuroscience2016
Gene expression elucidates functional impact of polygenic risk for schizophrenia.
Article in Nature neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 675 papers, 7 of them syntheses that pooled it.
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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.
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Who cites it
675 citing papers in PubMed, 7 syntheses or guidelines pooled it, 1,199 citations in OpenAlex.
- Multi-Trait Genetic Insights Into Schizophrenia Across Ancestries: Genome-Wide Association Meta-Analyses, Machine Learning, and Drug Repurposing Study.Brain and behavior · 2026Pooled it
- A meta-analysis of single-nucleus expression quantitative trait loci linking genetic risk to brain disorders.Nature genetics · 2026Pooled it
- Sex-stratified genome-wide association meta-analysis of major depressive disorder.Nature communications · 2025Pooled it
- A contextual genomic perspective on physical activity and its relationship to health, well being and illness.Nature genetics · 2025Pooled it
- A multi-ancestry genetic study of pain intensity in 598,339 veterans.Nature medicine · 2024Pooled it
- Genome-wide meta-analysis, functional genomics and integrative analyses implicate new risk genes and therapeutic targets for anxiety disorders.Nature human behaviour · 2024Pooled it
- Genome-wide association study in 404,302 individuals identifies 7 significant loci for reaction time variability.Molecular psychiatry · 2023Pooled it
- Article
- Distinct contributions of schizophrenia and neurotransmitter pathway genetic liability to neurocognition and antipsychotic efficacy in drug-naïve first-episode schizophrenia.Molecular psychiatry · 2026Article
- Single-nucleus atlas of cell-type specific genetic regulation in the human brain.Nature genetics · 2026Article
- Estimating protein isoform abundances with [Formula: see text].Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Exploring the shared genetic architecture and causal relationship between childhood maltreatment and psychiatric disorders.Molecular psychiatry · 2026Article
- Genome-wide tandem repeat expansions modify schizophrenia risk in the presence of a 22q11.2 deletion.Molecular psychiatry · 2026Article
- Dynamic neuro-immune regulation of psychiatric risk loci in human neurons.Nature communications · 2026Article
- Article
- Glutamatergic Modulators in Schizophrenia: Are We Ready to Move Beyond the Narrow Focus on Dopamine? A Potential Paradigm Shift in Psychopharmacology.Alpha psychiatry · 2026Article
- Analysis of gene co-expression connectivity dynamics implicates aberrant neuron-oligodendroglia interactions in schizophrenia.Nature communications · 2026Article
- Mapping lncRNAs onto multilevel mRNA co‑expression modules in autism.Translational psychiatry · 2026Article
- Data-intensive immune network modelling for One Health.Briefings in bioinformatics · 2026Review
- Co-expression-based models improve eQTL predictions for transcriptome-wide association studies and highlight new schizophrenia-associated genes.Nature genetics · 2026Article
615 more citing papers are in PubMed but not listed here.
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Authors and funding
58 authors at 16 institutions in 4 countries.
Funding
Abstract
Over 100 genetic loci harbor schizophrenia-associated variants, yet how these variants confer liability is uncertain. The CommonMind Consortium sequenced RNA from dorsolateral prefrontal cortex of people with schizophrenia (N = 258) and control subjects (N = 279), creating a resource of gene expression and its genetic regulation. Using this resource, ∼20% of schizophrenia loci have variants that could contribute to altered gene expression and liability. In five loci, only a single gene was involved: FURIN, TSNARE1, CNTN4, CLCN3 or SNAP91. Altering expression of FURIN, TSNARE1 or CNTN4 changed neurodevelopment in zebrafish; knockdown of FURIN in human neural progenitor cells yielded abnormal migration. Of 693 genes showing significant case-versus-control differential expression, their fold changes were ≤ 1.33, and an independent cohort yielded similar results. Gene co-expression implicates a network relevant for schizophrenia. Our findings show that schizophrenia is polygenic and highlight the utility of this resource for mechanistic interpretations of genetic liability for brain diseases.
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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.