Evidence map›Paper›PMID 39358328›Full record

ArticleTranslational psychiatry2024

Associations between antagonistic SNPs for neuropsychiatric disorders and human brain structure.

Lydia M Federmann, Friederike S David, Christiane Jockwitz, Thomas W Mühleisen, Dominique I Pelzer, Markus M Nöthen, Svenja Caspers, Katrin Amunts, Janik Goltermann, Till F M Andlauer and 7 more

Abstract read
In one paragraph

Article in Translational psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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.

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Lydia M FedermannInstitute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany. l.federmann@fz-juelich.de.ORCID 0009-0006-4500-2175
Friederike S DavidInstitute of Human Genetics, University of Bonn, School of Medicine & University Hospital Bonn, Bonn, Germany.ORCID 0000-0001-9521-5669
Christiane JockwitzInstitute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany.
Thomas W MühleisenInstitute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany.ORCID 0000-0002-6057-5952
Dominique I PelzerInstitute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany.ORCID 0000-0003-3360-5754
Markus M NöthenInstitute of Human Genetics, University of Bonn, School of Medicine & University Hospital Bonn, Bonn, Germany.ORCID 0000-0002-8770-2464
Svenja CaspersInstitute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany.
Katrin AmuntsInstitute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany.ORCID 0000-0001-5828-0867
Janik GoltermannInstitute for Translational Psychiatry, University of Münster, Münster, Germany.
Till F M AndlauerDepartment of Neurology, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany.ORCID 0000-0002-2917-5889
Frederike SteinDepartment of Psychiatry and Psychotherapy, Philipps-University and University Hospital Marburg, Marburg, Germany.
Katharina BroschDepartment of Psychiatry and Psychotherapy, Philipps-University and University Hospital Marburg, Marburg, Germany.ORCID 0000-0002-0526-8095
Tilo KircherDepartment of Psychiatry and Psychotherapy, Philipps-University and University Hospital Marburg, Marburg, Germany.
Sven CichonInstitute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany.ORCID 0000-0002-9475-086X
Udo DannlowskiInstitute for Translational Psychiatry, University of Münster, Münster, Germany.
Lisa Sindermann *Institute of Human Genetics, University of Bonn, School of Medicine & University Hospital Bonn, Bonn, Germany.
Andreas J Forstner *Institute of Neuroscience and Medicine (INM-1), Research Centre Jülich, Jülich, Germany. a.forstner@fz-juelich.de.ORCID 0000-0002-1876-6368

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) DA1151/5-1Deutsche Forschungsgemeinschaft (German Research Foundation) DA1151/5-2Deutsche Forschungsgemeinschaft (German Research Foundation) KI588/14-1Deutsche Forschungsgemeinschaft (German Research Foundation) KI588/14-2Deutsche Forschungsgemeinschaft (German Research Foundation) KI588/20-1Deutsche Forschungsgemeinschaft (German Research Foundation) KI588/22-1Deutsche Forschungsgemeinschaft (German Research Foundation) NO 246/10-1Deutsche Forschungsgemeinschaft (German Research Foundation) NO 246/10-2
6 · The paper itself

Abstract

A previously published genome-wide association study (GWAS) meta-analysis across eight neuropsychiatric disorders identified antagonistic single-nucleotide polymorphisms (SNPs) at eleven genomic loci where the same allele was protective against one neuropsychiatric disorder and increased the risk for another. Until now, these antagonistic SNPs have not been further investigated regarding their link to brain structural phenotypes. Here, we explored their associations with cortical surface area and cortical thickness (in 34 brain regions and one global measure each) as well as the volumes of eight subcortical structures using summary statistics of large-scale GWAS of brain structural phenotypes. We assessed if significantly associated brain structural phenotypes were previously reported to be associated with major neuropsychiatric disorders in large-scale case-control imaging studies by the ENIGMA consortium. We further characterized the effects of the antagonistic SNPs on gene expression in brain tissue and their association with additional cognitive and behavioral phenotypes, and performed an exploratory voxel-based whole-brain analysis in the FOR2107 study (n = 754 patients with major depressive disorder and n = 847 controls). We found that eight antagonistic SNPs were significantly associated with brain structural phenotypes in regions such as anterior parts of the cingulate cortex, the insula, and the superior temporal gyrus. Case-control differences in implicated brain structural phenotypes have previously been reported for bipolar disorder, major depressive disorder, and schizophrenia. In addition, antagonistic SNPs were associated with gene expression changes in brain tissue and linked to several cognitive-behavioral traits. In our exploratory whole-brain analysis, we observed significant associations of gray matter volume in the left superior temporal pole and left superior parietal region with the variants rs301805 and rs1933802, respectively. Our results suggest that multiple antagonistic SNPs for neuropsychiatric disorders are linked to brain structural phenotypes. However, to further elucidate these findings, future case-control genomic imaging studies are required.

Indexed as

BrainGenome-Wide Association StudyMajor Depressive DisorderPolymorphism, Single NucleotideAdultCase-Control StudiesFemaleGenetic Predisposition to DiseaseHumansMagnetic Resonance ImagingMaleMental DisordersMiddle AgedPhenotype

Identifiers

PMID39358328
PMCPMC11446931

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