Evidence map›Paper›PMID 29500446›Full record

ArticleScientific reports2018

Significance of risk polymorphisms for depression depends on stress exposure.

Xenia Gonda, Gabor Hullam, Peter Antal, Nora Eszlari, Peter Petschner, Tomas Gm Hökfelt, Ian Muir Anderson, John Francis William Deakin, Gabriella Juhasz, Gyorgy Bagdy

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

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  9. Facing stress and inflammation: From the cell to the planet.World journal of experimental medicine · 2024
    Review
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  15. Treatment-Resistant Depression Revisited: A Glimmer of Hope.Journal of personalized medicine · 2021
    Review
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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

10 authors at 5 institutions in 3 countries.

Xenia GondaDepartment of Psychiatry and Psychotherapy, Semmelweis University, Budapest, Hungary. gonda.xenia@med.semmelweis-univ.hu.ORCID 0000-0001-9015-4203
Gabor HullamMTA-SE Neuropsychopharmacology and Neurochemistry Research Group, Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary.
Peter AntalDepartment of Measurement and Information Systems, Budapest University of Technology and Economics, Budapest, Hungary.ORCID 0000-0002-4370-2198
Nora EszlariMTA-SE Neuropsychopharmacology and Neurochemistry Research Group, Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary.
Peter PetschnerMTA-SE Neuropsychopharmacology and Neurochemistry Research Group, Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary.
Tomas Gm HökfeltRetzius Laboratory, Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Ian Muir AndersonNeuroscience and Psychiatry Unit, Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
John Francis William DeakinNeuroscience and Psychiatry Unit, Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.ORCID 0000-0002-2750-962X
Gabriella JuhaszMTA-SE Neuropsychopharmacology and Neurochemistry Research Group, Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary.
Gyorgy BagdyMTA-SE Neuropsychopharmacology and Neurochemistry Research Group, Hungarian Academy of Sciences, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUBudapest University of Technology and Economics · HUGreater Manchester Mental Health NHS Foundation Trust · GBKarolinska Institutet · SEManchester Academic Health Science Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depression is a polygenic and multifactorial disorder where environmental effects exert a significant impact, yet most genetic studies do not consider the effect of stressors which may be one reason for the lack of replicable results in candidate gene studies, GWAS and between human studies and animal models. Relevance of functional polymorphisms in seven candidate genes previously implicated in animal and human studies on a depression-related phenotype given various recent stress exposure levels was assessed with Bayesian relevance analysis in 1682 subjects. This Bayesian analysis indicated a gene-environment interaction whose significance was also tested with a traditional multivariate analysis using general linear models. The investigated genetic factors were only relevant in the moderate and/or high stress exposure groups. Rank order of genes was GALR2 > BDNF > P2RX7 > HTR1A > SLC6A4 > CB1 > HTR2A, with strong relevance for the first four. Robust gene-gene-environment interaction was found between BDNF and HTR1A. Gene-environment interaction effect was confirmed, namely no main effect of genes, but a significant modulatory effect on environment-induced development of depression were found. Our data support the strong causative role of the environment modified by genetic factors, similar to animal models. Gene-environment interactions point to epigenetic factors associated with risk SNPs. Galanin-2 receptor, BDNF and X-type purin-7 receptor could be drug targets for new antidepressants.

Indexed as

Genetic Predisposition to DiseaseStress, PsychologicalBayes TheoremDepressionFemaleGene-Environment InteractionHumansMalePolymorphism, Single Nucleotide

Identifiers

PMID29500446
PMCPMC5834495
OpenAlexW2805875476

What OpenQuestion holds

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LicenceCC BY
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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.