ArticleMolecular psychiatry2022
Predicting causal genes from psychiatric genome-wide association studies using high-level etiological knowledge.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
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Who cites it
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.
- Genome-wide analyses identify 30 loci associated with obsessive-compulsive disorder.Nature genetics · 2025Pooled it
- Pooled it
- Cross-ancestry genetic architecture reveals shared biological pathways of major psychiatric disorders.Molecular psychiatry · 2026Article
- Identifying drug targets for schizophrenia through gene prioritization.Translational psychiatry · 2026Article
- Shared genetics and causal relationship between sociability and the brain's default mode network.Psychological medicine · 2025Article
- Genome-wide analyses identify 30 loci associated with obsessive-compulsive disorder.medRxiv : the preprint server for health sciences · 2025Article
- Transcriptomic pathology of neocortical microcircuit cell types across psychiatric disorders.Molecular psychiatry · 2025Article
- Genetic implication of GABAFrontiers in pharmacology · 2025Review
- CACNA1C (CaNeuropharmacology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Genome-wide association studies have discovered hundreds of genomic loci associated with psychiatric traits, but the causal genes underlying these associations are often unclear, a research gap that has hindered clinical translation. Here, we present a Psychiatric Omnilocus Prioritization Score (PsyOPS) derived from just three binary features encapsulating high-level assumptions about psychiatric disease etiology - namely, that causal psychiatric disease genes are likely to be mutationally constrained, be specifically expressed in the brain, and overlap with known neurodevelopmental disease genes. To our knowledge, PsyOPS is the first method specifically tailored to prioritizing causal genes at psychiatric GWAS loci. We show that, despite its extreme simplicity, PsyOPS achieves state-of-the-art performance at this task, comparable to a prior domain-agnostic approach relying on tens of thousands of features. Genes prioritized by PsyOPS are substantially more likely than other genes at the same loci to have convergent evidence of direct regulation by the GWAS variant according to both DNA looping assays and expression or splicing quantitative trait locus (QTL) maps. We provide examples of genes hundreds of kilobases away from the lead variant, like GABBR1 for schizophrenia, that are prioritized by all three of PsyOPS, DNA looping and QTLs. Our results underscore the power of incorporating high-level knowledge of trait etiology into causal gene prediction at GWAS loci, and comprise a resource for researchers interested in experimentally characterizing psychiatric gene candidates.
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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 Socratic graph.