Evidence map›Paper›PMID 26899160›Full record

ArticleHuman genetics2016

Gene co-expression analysis identifies brain regions and cell types involved in migraine pathophysiology: a GWAS-based study using the Allen Human Brain Atlas.

Else Eising, Sjoerd M H Huisman, Ahmed Mahfouz, Lisanne S Vijfhuizen, Verneri Anttila, Bendik S Winsvold, Tobias Kurth, M Arfan Ikram, Tobias Freilinger, Jaakko Kaprio and 19 more

Open access · hybridAbstract read
In one paragraph

Article in Human genetics, 2016. 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
7.2field-weighted citation impact, top 2% 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.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The journal of headache and pain · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Genetics of migraine: where are we now?The journal of headache and pain · 2023
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Exploring the Hereditary Nature of Migraine.Neuropsychiatric disease and treatment · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. 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

29 authors at 20 institutions in 8 countries.

Else EisingDepartment of Human Genetics, Leiden University Medical Center, 2333 ZC, Leiden, The Netherlands.
Sjoerd M H HuismanDelft Bioinformatics Lab, Department of Intelligent Systems, Delft University of Technology, 2628 CD, Delft, The Netherlands.
Ahmed MahfouzDelft Bioinformatics Lab, Department of Intelligent Systems, Delft University of Technology, 2628 CD, Delft, The Netherlands.
Lisanne S VijfhuizenDepartment of Human Genetics, Leiden University Medical Center, 2333 ZC, Leiden, The Netherlands.
Verneri AnttilaAnalytical and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Bendik S WinsvoldFORMI and Department of Neurology, Oslo University Hospital and University of Oslo, 0424, Oslo, Norway.
Tobias KurthInstitute of Public Health, Charité - Universitätsmedizin Berlin, 10117, Berlin, Germany.
M Arfan IkramDepartment of Epidemiology, Erasmus University Medical Centre, 3015 CE, Rotterdam, The Netherlands.
Tobias FreilingerDepartment of Neurology and Epileptology and Hertie-Institute for Clinical Brain Research, University of Tübingen, 72076, Tübingen, Germany.
Jaakko KaprioDepartment of Public Health, University of Helsinki, 00014, Helsinki, Finland.
Dorret I BoomsmaDepartment of Biological Psychology, VU University, 1081 HV, Amsterdam, The Netherlands.
Cornelia M van DuijnDepartment of Epidemiology, Erasmus University Medical Centre, 3015 CE, Rotterdam, The Netherlands.
Marjo-Riitta R JärvelinDepartment of Epidemiology and Biostatistics, MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, London, W2 1PG, UK.
John-Anker ZwartFORMI and Department of Neurology, Oslo University Hospital and University of Oslo, 0424, Oslo, Norway.
Lydia QuayeDepartment of Twin Research and Genetic Epidemiology, King's College London, London, SE1 7EH, UK.
David P StrachanPopulation Health Research Institute, St George's, University of London, London, SW17 0RE, UK.
Christian KubischInstitute of Human Genetics, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Martin DichgansInstitute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximillians-Universität, 81377, Munich, Germany.
George Davey SmithMedical Research Council Integrative Epidemiology Unit (IEU), School of Social and Community Medicine, University of Bristol, Bristol, BS8 2PS, UK.
Kari StefanssondeCODE Genetics, 101, Reykjavik, Iceland.
Aarno PalotieAnalytical and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Daniel I ChasmanDivision of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02215-1204, USA.
Michel D FerrariDepartment of Neurology, Leiden University Medical Center, 2333 ZA, Leiden, The Netherlands.
Gisela M TerwindtDepartment of Neurology, Leiden University Medical Center, 2333 ZA, Leiden, The Netherlands.
Boukje de VriesDepartment of Human Genetics, Leiden University Medical Center, 2333 ZC, Leiden, The Netherlands.
Dale R NyholtInstitute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, QLD, Brisbane, QLD, 4059, Australia.
Boudewijn P F LelieveldtDelft Bioinformatics Lab, Department of Intelligent Systems, Delft University of Technology, 2628 CD, Delft, The Netherlands.
Arn M J M van den MaagdenbergDepartment of Human Genetics, Leiden University Medical Center, 2333 ZC, Leiden, The Netherlands. A.M.J.M.van_den_Maagdenberg@lumc.nl.
Marcel J T ReindersDelft Bioinformatics Lab, Department of Intelligent Systems, Delft University of Technology, 2628 CD, Delft, The Netherlands. m.j.t.reinders@tudelft.nl.
Leiden University Medical Center · NLDelft University of Technology · NLBrigham and Women's Hospital · USCharité - Universitätsmedizin Berlin · DEErasmus MC · NLErasmus University Rotterdam · NLHarvard University · USHertie Institute for Clinical Brain Research · DEInstitute for Molecular Medicine Finland · FIKing's College London · GBLudwig-Maximilians-Universität München · DEMassachusetts General Hospital · USMedical Research Council · GBOslo University Hospital · NOOulu University of Applied Sciences · FIQIMR Berghofer Medical Research Institute · AUSt George's, University of London · GBUniversität Hamburg · DEUniversity of Iceland · ISUniversity of Oslo · NO

Funding

The Women's Health Study: Infrastructure Support for Continued Cohort Follow-upUM1CA182913 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI BURING, JULIE E., LEE, I-MIN · 2014 to 2018
$4.0M
Medical Research Council G1001799Medical Research Council G9815508Medical Research Council MC_PC_15018Medical Research Council MC_UU_12013/1Medical Research Council MR/N01104X/1NCI NIH HHS UM1 CA182913Wellcome Trust 102215
6 · The paper itself

Abstract

Migraine is a common disabling neurovascular brain disorder typically characterised by attacks of severe headache and associated with autonomic and neurological symptoms. Migraine is caused by an interplay of genetic and environmental factors. Genome-wide association studies (GWAS) have identified over a dozen genetic loci associated with migraine. Here, we integrated migraine GWAS data with high-resolution spatial gene expression data of normal adult brains from the Allen Human Brain Atlas to identify specific brain regions and molecular pathways that are possibly involved in migraine pathophysiology. To this end, we used two complementary methods. In GWAS data from 23,285 migraine cases and 95,425 controls, we first studied modules of co-expressed genes that were calculated based on human brain expression data for enrichment of genes that showed association with migraine. Enrichment of a migraine GWAS signal was found for five modules that suggest involvement in migraine pathophysiology of: (i) neurotransmission, protein catabolism and mitochondria in the cortex; (ii) transcription regulation in the cortex and cerebellum; and (iii) oligodendrocytes and mitochondria in subcortical areas. Second, we used the high-confidence genes from the migraine GWAS as a basis to construct local migraine-related co-expression gene networks. Signatures of all brain regions and pathways that were prominent in the first method also surfaced in the second method, thus providing support that these brain regions and pathways are indeed involved in migraine pathophysiology.

Indexed as

Gene ExpressionGenome-Wide Association StudyAtlases as TopicBrainHumansMigraine Disorders

Identifiers

PMID26899160
PMCPMC4796339
OpenAlexW2280484307

What Socratic holds

Textmetadata
LicenceCC BY
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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.