Evidence map›Paper›PMID 31520123›Full record

ReviewHuman genetics2020

Discovery of shared genomic loci using the conditional false discovery rate approach.

Olav B Smeland, Oleksandr Frei, Alexey Shadrin, Kevin O'Connell, Chun-Chieh Fan, Shahram Bahrami, Dominic Holland, Srdjan Djurovic, Wesley K Thompson, Anders M Dale and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

175 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Identification ofFrontiers in immunology · 2026
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Article
  7. Article
  8. Eating Disorders and Parkinson's Disease-2: Genetic Epidemiology and Shared Genomics.European eating disorders review : the journal of the Eating Disorders Association · 2026
    Article
  9. Shared genetic architecture between DTI-ALPS traits and neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Shared genetic architecture and neurobiological pathways of problematic alcohol use and anxiety disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  16. Article
  17. Article
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  19. Genetic overlap between treatment-resistant schizophrenia and smoking initiation.The international journal of neuropsychopharmacology · 2026
    Article
  20. Article

115 more citing papers are in PubMed but not listed here.

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

11 authors.

Olav B SmelandNORMENT Centre, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0424, Oslo, Norway. o.b.smeland@medisin.uio.no.ORCID http://orcid.org/0000-0002-3761-5215
Oleksandr FreiNORMENT Centre, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0424, Oslo, Norway.ORCID http://orcid.org/0000-0002-6427-2625
Alexey ShadrinNORMENT Centre, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0424, Oslo, Norway.
Kevin O'ConnellNORMENT Centre, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0424, Oslo, Norway.ORCID http://orcid.org/0000-0002-6865-8795
Chun-Chieh FanDepartment of Cognitive Science, University of California San Diego, La Jolla, San Diego, CA, 92093, USA.ORCID http://orcid.org/0000-0001-9437-2128
Shahram BahramiNORMENT Centre, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0424, Oslo, Norway.
Dominic HollandDepartment of Radiology, University of California of San Diego, La Jolla, San Diego, CA, 92093, USA.
Srdjan DjurovicDepartment of Medical Genetics, Oslo University Hospital, Oslo, Norway.ORCID http://orcid.org/0000-0002-8140-8061
Wesley K ThompsonDepartment of Family Medicine and Public Health, University of California San Diego, La Jolla, San Diego, CA, 92093, USA.ORCID http://orcid.org/0000-0002-1148-1976
Anders M DaleDepartment of Cognitive Science, University of California San Diego, La Jolla, San Diego, CA, 92093, USA.ORCID http://orcid.org/0000-0002-6126-2966
Ole A AndreassenNORMENT Centre, Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0424, Oslo, Norway. o.a.andreassen@medisin.uio.no.ORCID http://orcid.org/0000-0002-4461-3568

Funding

ABCD-USA Consortium: Data Analysis, Informatics and Resource CenterU24DA041123 · NIDA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ANDERS M DALE · 2015 to 2026
$51.5M
Helse Sør-Øst RHF 2017-112NIDA NIH HHS U24DA041123NIH HHS EB00790NIH HHS NS057198Stiftelsen Kristian Gerhard Jebsen SKGJ-2011-36The Research Council of Norway 213837The Research Council of Norway 223273The Research Council of Norway 229129The Research Council of Norway 248778The Research Council of Norway 249711
6 · The paper itself

Abstract

In recent years, genome-wide association study (GWAS) sample sizes have become larger, the statistical power has improved and thousands of trait-associated variants have been uncovered, offering new insights into the genetic etiology of complex human traits and disorders. However, a large fraction of the polygenic architecture underlying most complex phenotypes still remains undetected. We here review the conditional false discovery rate (condFDR) method, a model-free strategy for analysis of GWAS summary data, which has improved yield of existing GWAS and provided novel findings of genetic overlap between a wide range of complex human phenotypes, including psychiatric, cardiovascular, and neurological disorders, as well as psychological and cognitive traits. The condFDR method was inspired by Empirical Bayes approaches and leverages auxiliary genetic information to improve statistical power for discovery of single-nucleotide polymorphisms (SNPs). The cross-trait condFDR strategy analyses separate GWAS data, and leverages overlapping SNP associations, i.e., cross-trait enrichment, to increase discovery of trait-associated SNPs. The extension of the condFDR approach to conjunctional FDR (conjFDR) identifies shared genomic loci between two phenotypes. The conjFDR approach allows for detection of shared genomic associations irrespective of the genetic correlation between the phenotypes, often revealing a mixture of antagonistic and agonistic directional effects among the shared loci. This review provides a methodological comparison between condFDR and other relevant cross-trait analytical tools and demonstrates how condFDR analysis may provide novel insights into the genetic relationship between complex phenotypes.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyMultifactorial InheritancePolymorphism, Single NucleotideGenomicsHumansPhenotype

Identifiers

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.