This article is part of the supplement: Abstract Book of The European Headache and Migraine Trust International Congress

Open Access Poster presentation

Migraine without aura: genome-wide association analysis identifies several novel susceptibility

B L De Vries1*, T Freilinger2, V Anttila3, R Malik2, GM Terwindt4, P Pozo-Rosich5, B Winsvold6, D Nyholt7, WPJ van Oosterhout8, V Artto9, M Todt10, E Hämäläinen3, J Fernandez-Moralez3, M Louter8, MA Kaunisto11, J Schoenen12, O Raitakari13, T Lehtimäki14, M Ville-Pueyo15, H Göbel16, E Wichman17, C Sintas18, A Uitterlinden19, A Hofman20, F Rivadeneira19, A Heinze16, E Tronvik21, CM van Duin20, J Kaprio22, B Cormand18, M Wessman22, RR Frants1, T Meitinger23, B Müller-Myhsok24, JA Zwart25, M Färkkilä9, A Macaya15, MD Ferrari4, C Kubisch10, A Palotie3, M Dichgans2 and AMJ van den Maagdenberg1

  • * Corresponding author: B L De Vries

Author Affiliations

1 Department of Human Genetics, Leiden University Medical Centre (LUMC), Netherlands

2 Institute for Stroke and Dementia Research, Klinikum der Universität München, Munich, Germany

3 Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, UK

4 Department of Neurology, Leiden University Medical Centre (LUMC), Netherlands

5 Department of Neurology, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Spain

6 Department of Neurology, Oslo University Hospital and University of Oslo, Norway

7 Neurogenetics Laboratory, Queensland Institute of Medical Research, Brisbane, Australia

8 Department of Neurology, Leiden Medical Centre (LUMC), Netherlands

9 Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland

10 Institute of Human Genetics, University of Ulm, Germany

11 Institute for Molecular Medicine Finland (FIMM), University of Helsinki, UK

12 Headache Research Unit, Department of Neurology and Groupe Interdisciplinaire de Génoprotéomique Appliquée (GIGA)-Neurosciences, Belgium

13 Department of Clinical Physiology, University of Turku and Turku University Central Hospital, Turku, Finland

14 Department of Clinical Chemistry, Tampere University Hospital and University of Tampere, Tampere, Finland

15 Pediatric Neurology Research Group, Vall d'Hebron Research Institute, Barcelona, Spain

16 Kiel Pain and Headache Center, Kiel, Germany

17 Institute of Epidemiology, Helmholtz Center Munich, Neuherberg, Germany

18 Department of Genetics, University of Barcelona, Barcelona, Spain

19 Department of Internal Medicine, Erasmus Medical Center, Rotterdam, Netherlands

20 Department of Epidemiology, Erasmus University Medical Center, Rotterdam, Netherlands

21 Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway

22 Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland

23 Institute of Human Genetics, Helmholtz Zentrum München, Neuherberg, Germany

24 Max Planck Institute of Psychiatry, Munich, Germany

25 Oslo University Hospital and University of Oslo, Norway

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The Journal of Headache and Pain 2013, $article.volume.volumeNumber(Suppl 1):P21 doi:10.1186/1129-2377-1-S1-P21


The electronic version of this article is the complete one and can be found online at: http://www.thejournalofheadacheandpain.com/content/1/S1/P21


Published:21 February 2013

© 2013 De Vries et al; licensee Springer.

Introduction

Genome-wide association studies (GWAS) are a novel and promising method to study genetic susceptibility factors for common disorders, including migraine.

Objective

Here we performed the first GWAS in migraine without aura (MO), which is the most common form of migraine.

Methods

To identify common genetic variants for this migraine type, we analyzed genome-wide association data of 2,326 clinic-based German and Dutch patients and 4,580 population-matched controls. Loci with two or more SNPs with P-values < 1 x 10-5 were selected for follow-up in 2,508 Dutch, Spanish, Finnish and Norwegian patients and 2,652 controls.

Results

Meta-analysis of the discovery and replication data yielded four genome-wide significant (P < 5 x 10-8) MO susceptibility loci in or nearby MEF2D, PHACTR1, ASTN2 and TGFBR2. In addition, SNPs in two loci (in or near TRPM8 and LRP1) that were previously identified in a GWAS on population-based migraine were significantly replicated in our clinic-based MO cohort.

Conclusion

This study reveals the first susceptibility loci for migraine without aura, thereby expanding our knowledge of this debilitating neurological disorder.