Kaya K Jacobsen1, Caroline M Nievergelt2, Tetyana Zayats3, Tiffany A Greenwood2, Verneri Anttila4, Hagop S Akiskal5, Jan Haavik6, Ole Bernt Fasmer7, John R Kelsoe5, Stefan Johansson8, Ketil J Oedegaard7. 1. KG Jebsen Center for Neurophyciatric research, Department of Biomedicine, University of Bergen, Bergen, Norway; Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway. Electronic address: kja098@biomed.uib.no. 2. Department of Psychiatry, University of California, San Diego, USA. 3. KG Jebsen Center for Neurophyciatric research, Department of Biomedicine, University of Bergen, Bergen, Norway; Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway. 4. Analytical and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA; Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland. 5. Department of Psychiatry, University of California, San Diego, USA; Department of Psychiatry, VA Hospital, San Diego, USA. 6. KG Jebsen Center for Neurophyciatric research, Department of Biomedicine, University of Bergen, Bergen, Norway; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway. 7. KG Jebsen Center for Neurophyciatric research, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway. 8. KG Jebsen Center for Neurophyciatric research, Department of Biomedicine, University of Bergen, Bergen, Norway; Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway; Department of Clinical Science, University of Bergen, Norway.
Abstract
BACKGROUND: Migraine is a common comorbidity among individuals with bipolar disorder, but the underlying mechanisms for this co-occurrence are poorly understood. The aim of this study was to investigate the genetic background of bipolar patients with and without migraine. METHODS: We performed a genome-wide association analysis contrasting 460 bipolar migraneurs with 914 bipolar patients without migraine from the Bipolar Genome Study (BiGS). RESULTS: We identified one genome-wide significant association between migraine in bipolar disorder patients and rs1160720, an intronic single nucleotide polymorphism (SNP) in the NBEA gene (P=2.97 × 10(-8), OR: 1.82, 95% CI: 1.47-2.25), although this was not replicated in a smaller sample of 289 migraine cases. LIMITATIONS: Our study is based on self-reported migraine. CONCLUSIONS: NBEA encodes neurobeachin, a scaffolding protein primarily expressed in the brain and involved in trafficking of vesicles containing neurotransmitter receptors. This locus has not previously been implicated in migraine per se. We found no evidence of association in data from the GWAS migraine meta-analysis consortium (n=118,710 participants) suggesting that the association might be specific to migraine co-morbid with bipolar disorder.
BACKGROUND:Migraine is a common comorbidity among individuals with bipolar disorder, but the underlying mechanisms for this co-occurrence are poorly understood. The aim of this study was to investigate the genetic background of bipolarpatients with and without migraine. METHODS: We performed a genome-wide association analysis contrasting 460 bipolar migraneurs with 914 bipolarpatients without migraine from the Bipolar Genome Study (BiGS). RESULTS: We identified one genome-wide significant association between migraine in bipolar disorderpatients and rs1160720, an intronic single nucleotide polymorphism (SNP) in the NBEA gene (P=2.97 × 10(-8), OR: 1.82, 95% CI: 1.47-2.25), although this was not replicated in a smaller sample of 289 migraine cases. LIMITATIONS: Our study is based on self-reported migraine. CONCLUSIONS:NBEA encodes neurobeachin, a scaffolding protein primarily expressed in the brain and involved in trafficking of vesicles containing neurotransmitter receptors. This locus has not previously been implicated in migraine per se. We found no evidence of association in data from the GWAS migraine meta-analysis consortium (n=118,710 participants) suggesting that the association might be specific to migraine co-morbid with bipolar disorder.
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