Evidence map›Paper›PMID 35411039›Full record

ArticleMolecular psychiatry2022

Predicting causal genes from psychiatric genome-wide association studies using high-level etiological knowledge.

Michael Wainberg, Daniele Merico, Matthew C Keller, Eric B Fauman, Shreejoy J Tripathy

Abstract read
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In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Genome-wide analyses identify 30 loci associated with obsessive-compulsive disorder.medRxiv : the preprint server for health sciences · 2025
    Article
  7. Article
  8. Genetic implication of GABAFrontiers in pharmacology · 2025
    Review
  9. CACNA1C (CaNeuropharmacology · 2022
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Michael WainbergKrembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada.ORCID http://orcid.org/0000-0001-6061-0239
Daniele MericoDeep Genomics Inc, Toronto, ON, Canada.ORCID http://orcid.org/0000-0002-3728-4401
Matthew C KellerDepartment of Psychology and Neuroscience, University of Colorado, Boulder, CO, USA.ORCID http://orcid.org/0000-0002-6075-9882
Eric B FaumanInternal Medicine Research Unit, Pfizer Worldwide Research, Development and Medical, Cambridge, MA, USA.ORCID http://orcid.org/0000-0002-9739-0249
Shreejoy J TripathyKrembil Centre for Neuroinformatics, Centre for Addiction and Mental Health, Toronto, ON, Canada. shreejoy.tripathy@utoronto.ca.
Centre for Addiction and Mental Health · CAHospital for Sick Children · CAPfizer (United States) · USUniversity of Colorado Boulder · US

Funding

CIHR NGN-171423
6 · The paper itself

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.

Indexed as

Genome-Wide Association StudyQuantitative Trait LociDNAGenetic Predisposition to DiseaseGenomicsHumansPhenotypePolymorphism, Single NucleotideDNA

Identifiers

PMID35411039
OpenAlexW4223536359

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.