ArticleNature genetics2019
Synergistic effects of common schizophrenia risk variants.
Article in Nature genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 4 of them syntheses that pooled 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.
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.
Who cites it
156 citing papers in PubMed, 4 syntheses or guidelines pooled it, 255 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
- Altered gene expression and PTSD symptom dimensions in World Trade Center responders.Molecular psychiatry · 2022Pooled it
- Multi-ancestry eQTL meta-analysis of human brain identifies candidate causal variants for brain-related traits.Nature genetics · 2022Pooled it
- Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology.Nature genetics · 2021Pooled it
- Model Systems infrastructure of the German Center for Mental Health (DZPG): toward an integrated, mechanism-based framework for mental health research.European archives of psychiatry and clinical neuroscience · 2026Review
- Convergent mitochondrial impairment and apoptosis driven by simultaneous down-regulation of multiple genes at 11p11.2 in Alzheimer's disease.Molecular psychiatry · 2026Article
- Exploring the shared genetic architecture and causal relationship between childhood maltreatment and psychiatric disorders.Molecular psychiatry · 2026Article
- Mechanical Stretch Disrupts Calcium Dynamics and Redistributes Piezo1 in Human Astrocytes.Annals of biomedical engineering · 2026Article
- Schizophrenia risk gene ZNF804A controls ribosome localization and synaptogenesis in developing human neurons.Science advances · 2026Article
- Functional impact of genetic background on variable expressivity in neurodevelopmental disorders.Nature communications · 2026Article
- Transcriptomic and phenotypic convergence of neurodevelopmental disorder risk genes in vitro and in vivo.Nature neuroscience · 2026Article
- 3D genetic architecture of schizophrenia risk across three neuronal subtypes.Molecular psychiatry · 2026Article
- Phosphatase Signaling as a Therapeutic Strategy in Schizophrenia.International journal of molecular sciences · 2026Review
- Multimodal bioinformatic analyses of genome-scale expression beyond gene-centric differential expression.Briefings in bioinformatics · 2026Review
- The polygenic, omnigenic and stratagenic models of complex disease risk.Nature genetics · 2026Review
- Kv11.1 (hERG) Protein Interaction Networks Connect Endocytic Trafficking to Polygenic Influences on Cardiac Repolarization.bioRxiv : the preprint server for biology · 2026Article
- Functional implications of polygenic risk for schizophrenia in human neurons.Nature communications · 2026Article
- A new perspective on population genetics: Deciphering the relationship between genetic variants and disease prevalence in Psoriasis.PloS one · 2026Article
- Inducible chromosomal rearrangement reveals nonlinear polygenic dosage effects in driving aneuploid yeast traits.Nature communications · 2025Article
- Exploring Random Forest in Genetic Risk Score Construction.Genetic epidemiology · 2025Article
96 more citing papers are in PubMed but not listed here.
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Authors and funding
25 authors at 5 institutions in 1 country.
Funding
Abstract
The mechanisms by which common risk variants of small effect interact to contribute to complex genetic disorders are unclear. Here, we apply a genetic approach, using isogenic human induced pluripotent stem cells, to evaluate the effects of schizophrenia (SZ)-associated common variants predicted to function as SZ expression quantitative trait loci (eQTLs). By integrating CRISPR-mediated gene editing, activation and repression technologies to study one putative SZ eQTL (FURIN rs4702) and four top-ranked SZ eQTL genes (FURIN, SNAP91, TSNARE1 and CLCN3), our platform resolves pre- and postsynaptic neuronal deficits, recapitulates genotype-dependent gene expression differences and identifies convergence downstream of SZ eQTL gene perturbations. Our observations highlight the cell-type-specific effects of common variants and demonstrate a synergistic effect between SZ eQTL genes that converges on synaptic function. We propose that the links between rare and common variants implicated in psychiatric disease risk constitute a potentially generalizable phenomenon occurring more widely in complex genetic disorders.
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Registered trials
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.