Evidence map›Paper›PMID 31748543›Full record

ArticleTranslational psychiatry2019

Identification of novel common variants associated with chronic pain using conditional false discovery rate analysis with major depressive disorder and assessment of pleiotropic effects of LRFN5.

Keira J A Johnston, Mark J Adams, Barbara I Nicholl, Joey Ward, Rona J Strawbridge, Andrew M McIntosh, Daniel J Smith, Mark E S Bailey

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

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  8. Two polygenic mouse models of major depressive disorders identify TMEM161B as a potential biomarker of disease in humans.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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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

8 authors at 4 institutions in 2 countries.

Keira J A JohnstonInstitute of Health and Wellbeing, University of Glasgow, Scotland, UK. k.johnston.2@research.gla.ac.uk.ORCID http://orcid.org/0000-0002-1370-3149
Mark J AdamsDivision of Psychiatry, University of Edinburgh, Scotland, UK.ORCID http://orcid.org/0000-0002-3599-6018
Barbara I NichollInstitute of Health and Wellbeing, University of Glasgow, Scotland, UK.
Joey WardInstitute of Health and Wellbeing, University of Glasgow, Scotland, UK.
Rona J StrawbridgeInstitute of Health and Wellbeing, University of Glasgow, Scotland, UK.ORCID http://orcid.org/0000-0001-8506-3585
Andrew M McIntoshDivision of Psychiatry, University of Edinburgh, Scotland, UK.ORCID http://orcid.org/0000-0002-0198-4588
Daniel J SmithInstitute of Health and Wellbeing, University of Glasgow, Scotland, UK.
Mark E S BaileySchool of Life Sciences, College of Medical, Veterinary & Life Sciences, University of Glasgow, Scotland, UK.ORCID http://orcid.org/0000-0002-9788-2278
University of Glasgow · GBUniversity of Edinburgh · GBKarolinska Institutet · SEKingston University · GB

Funding

British Heart FoundationDepartment of HealthMedical Research Council MC_PC_17209Medical Research Council MC_PC_17217Medical Research Council MR/N013166/1Medical Research Council MR/S003061/1Wellcome TrustWellcome Trust 104036/Z/14/Z
6 · The paper itself

Abstract

Chronic pain is a complex trait that is moderately heritable and genetically, as well as phenotypically, correlated with major depressive disorder (MDD). Use of the conditional false discovery rate (cFDR) approach, which leverages pleiotropy identified from existing GWAS outputs, has been successful in discovering novel associated variants in related phenotypes. Here, genome-wide association study outputs for both von Korff chronic pain grade and for MDD were used to identify variants meeting a cFDR threshold for each outcome phenotype separately, as well as a conjunctional cFDR (ccFDR) threshold for both phenotypes together. Using a moderately conservative threshold, we identified a total of 11 novel single nucleotide polymorphisms (SNPs), six of which were associated with chronic pain grade and nine of which were associated with MDD. Four SNPs on chromosome 14 were associated with both chronic pain grade and MDD. SNPs associated only with chronic pain grade were located within SLC16A7 on chromosome 12. SNPs associated only with MDD were located either in a gene-dense region on chromosome 1 harbouring LINC01360, LRRIQ3, FPGT and FPGT-TNNI3K, or within/close to LRFN5 on chromosome 14. The SNPs associated with both outcomes were also located within LRFN5. Several of the SNPs on chromosomes 1 and 14 were identified as being associated with expression levels of nearby genes in the brain and central nervous system. Overall, using the cFDR approach, we identified several novel genetic loci associated with chronic pain and we describe likely pleiotropic effects of a recently identified MDD locus on chronic pain.

Indexed as

Genetic PleiotropyGenetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentAdultCell Adhesion Molecules, NeuronalChildChild, PreschoolChronic PainFalse Positive ReactionsFemaleGenetic LociGenome-Wide Association StudyHumansInfantInfant, NewbornCell Adhesion Molecules, NeuronalLRFN5 protein, human

Identifiers

PMID31748543
PMCPMC6868167
OpenAlexW2990959498

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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.