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2 results on '"Hamalainen, Eija"'

1. Genome-wide meta-analysis identifies new susceptibility loci for migraine.

Author

Anttila V, Winsvold BS, Gormley P, Kurth T, Bettella F, McMahon G, Kallela M, Malik R, de Vries B, Terwindt G, Medland SE, Todt U, McArdle WL, Quaye L, Koiranen M, Ikram MA, Lehtimäki T, Stam AH, Ligthart L, Wedenoja J, Dunham I, Neale BM, Palta P, Hamalainen E, Schürks M, Rose LM, Buring JE, Ridker PM, Steinberg S, Stefansson H, Jakobsson F, Lawlor DA, Evans DM, Ring SM, Färkkilä M, Artto V, Kaunisto MA, Freilinger T, Schoenen J, Frants RR, Pelzer N, Weller CM, Zielman R, Heath AC, Madden PAF, Montgomery GW, Martin NG, Borck G, Göbel H, Heinze A, Heinze-Kuhn K, Williams FMK, Hartikainen AL, Pouta A, van den Ende J, Uitterlinden AG, Hofman A, Amin N, Hottenga JJ, Vink JM, Heikkilä K, Alexander M, Muller-Myhsok B, Schreiber S, Meitinger T, Wichmann HE, Aromaa A, Eriksson JG, Traynor B, Trabzuni D, Rossin E, Lage K, Jacobs SBR, Gibbs JR, Birney E, Kaprio J, Penninx BW, Boomsma DI, van Duijn C, Raitakari O, Jarvelin MR, Zwart JA, Cherkas L, Strachan DP, Kubisch C, Ferrari MD, van den Maagdenberg AMJM, Dichgans M, Wessman M, Smith GD, Stefansson K, Daly MJ, Nyholt DR, Chasman D, and Palotie A

Subjects
Cerebellum metabolism, Computational Biology, Frontal Lobe metabolism, Humans, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Migraine Disorders genetics
Abstract

Migraine is the most common brain disorder, affecting approximately 14% of the adult population, but its molecular mechanisms are poorly understood. We report the results of a meta-analysis across 29 genome-wide association studies, including a total of 23,285 individuals with migraine (cases) and 95,425 population-matched controls. We identified 12 loci associated with migraine susceptibility (P<5×10(-8)). Five loci are new: near AJAP1 at 1p36, near TSPAN2 at 1p13, within FHL5 at 6q16, within C7orf10 at 7p14 and near MMP16 at 8q21. Three of these loci were identified in disease subgroup analyses. Brain tissue expression quantitative trait locus analysis suggests potential functional candidate genes at four loci: APOA1BP, TBC1D7, FUT9, STAT6 and ATP5B.

Published
2013
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2. Shared genetic risk between migraine and coronary artery disease:A genome-wide analysis of common variants

Author

Winsvold, Bendik S., Bettella, Francesco, Witoelar, Aree, Anttila, Verneri, Gormley, Padhraig, Kurth, Tobias, Terwindt, Gisela M., Freilinger, Tobias, Frei, Oleksander, Shadrin, Alexey, Wang, Yunpeng, Dale, Anders M., van den Maagdenberg, Arn M.J.M., Nyholt, Dale R., Palotie, Aarno, Andreassen, Ole A., Zwart, John Anker, Artto, Ville, Belin, Andrea Carmine, Boomsma, Dorret I., Børte, Sigrid, Chasman, Daniel I., Cherkas, Lynn, Christensen, Anne Francke, Cormand, Bru, Cuenca-Leon, Ester, Davey-Smith, George, Dichgans, Martin, van Duijn, Cornelia, Eising, Else, Esko, Tonu, Esserlind, Ann Louise, Ferrari, Michel, Frants, Rune R., Furlotte, Nick, Griffiths, Lyn, Hamalainen, Eija, Hansen, Thomas Folkmann, Hiekkala, Marjo, Arfan Ikram, M., Ingason, Andres, Järvelin, Marjo Riitta, Kajanne, Risto, Kallela, Mikko, Kaprio, Jaakko, Kaunisto, Mari, Kubisch, Christian, Kurki, Mitja, Olesen, Jes, and Yao, Yong-Gang

Subjects
0301 basic medicine, Male, Epidemiology, Genome-wide association study, Disease, Coronary Artery Disease, Pathology and Laboratory Medicine, Bioinformatics, Cardiovascular, Vascular Medicine, Migraines, Medicine and Health Sciences, Coronary Heart Disease, 2.1 Biological and endogenous factors, Aetiology, Genetics, Multidisciplinary, Headaches, Pain Research, International Headache Genetics Consortium, Genomics, Single Nucleotide, Phenotype, Heart Disease, Genetic Epidemiology, Medicine, Medical genetics, Female, Pathogens, Chronic Pain, Research Article, Biotechnology, medicine.medical_specialty, General Science & Technology, Science, Migraine Disorders, Cardiology, Single-nucleotide polymorphism, Biology, Polymorphism, Single Nucleotide, Molecular Genetics, 03 medical and health sciences, Signs and Symptoms, Diagnostic Medicine, Clinical Research, Genome-Wide Association Studies, medicine, SNP, Humans, Genetic Predisposition to Disease, Polymorphism, Molecular Biology, Migraine, Heart Disease - Coronary Heart Disease, Genetic association, Clinical Genetics, Prevention, Human Genome, Biology and Life Sciences, Computational Biology, Human Genetics, Genome Analysis, medicine.disease, Atherosclerosis, Brain Disorders, 030104 developmental biology, Genetic epidemiology, Genetic Loci, Genome-Wide Association Study
Abstract

Migraine is a recurrent pain condition traditionally viewed as a neurovascular disorder, but little is known of its vascular basis. In epidemiological studies migraine is associated with an increased risk of cardiovascular disease, including coronary artery disease (CAD), suggesting shared pathogenic mechanisms. This study aimed to determine the genetic overlap between migraine and CAD, and to identify shared genetic risk loci, utilizing a conditional false discovery rate approach and data from two large-scale genome-wide association studies (GWAS) of CAD (C4D, 15,420 cases, 15,062 controls; CARDIoGRAM, 22,233 cases, 64,762 controls) and one of migraine (22,120 cases, 91,284 controls). We found significant enrichment of genetic variants associated with CAD as a function of their association with migraine, which was replicated across two independent CAD GWAS studies. One shared risk locus in the PHACTR1 gene (conjunctional false discovery rate for index SNP rs9349379 < 3.90 x 10−5), which was also identified in previous studies, explained much of the enrichment. Two further loci (in KCNK5 and AS3MT) showed evidence for shared risk (conjunctional false discovery rate < 0.05). The index SNPs at two of the three loci had opposite effect directions in migraine and CAD. Our results confirm previous reports that migraine and CAD share genetic risk loci in excess of what would be expected by chance, and highlight one shared risk locus in PHACTR1. Understanding the biological mechanisms underpinning this shared risk is likely to improve our understanding of both disorders. © 2017 Winsvold et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Published
2017

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