Genetic analysis for a shared biological basis between migraine and coronary artery disease

被引：57

作者：

Winsvold, Bendik S. ^{[1
,2
,3
,4
]}

Nelson, Christopher P. ^{[5
,6
]}

Malik, Rainer ^{[7
,8
]}

Gormley, Padhraig ^{[4
,9
,11
]}

Anttila, Verneri ^{[4
,9
,10
,12
,17
,18
]}

Vander Heiden, Jason ^{[19
]}

Elliott, Katherine S. ^{[21
]}

Jacobsen, Line M. ^{[2
]}

Palta, Priit ^{[4
,23
,24
]}

Amin, Najaf ^{[25
]}

de Vries, Boukje ^{[28
]}

Hamalainen, Eija ^{[4
,23
,24
]}

Freilinger, Tobias ^{[7
,30
,31
]}

Ikram, M. Arfan ^{[25
,26
,27
]}

Kessler, Thorsten ^{[32
,33
]}

Koiranen, Markku ^{[34
]}

Ligthart, Lannie ^{[36
,37
]}

McMahon, George ^{[38
]}

Pedersen, Linda M. ^{[2
]}

Willenborg, Christina ^{[39
,40
]}

Won, Hong-Hee ^{[9
,13
,14
,17
,18
]}

Olesen, Jes ^{[41
]}

Artto, Ville ^{[42
]}

Assimes, Themistocles L. ^{[43
]}

Blankenberg, Stefan ^{[44
]}

Boomsma, Dorret I. ^{[36
]}

Cherkas, Lynn ^{[45
]}

Smith, George Davey ^{[38
]}

Epstein, Stephen E. ^{[46
]}

Erdmann, Jeanette ^{[39
,40
]}

Ferrari, Michel D. ^{[29
]}

Gobel, Hartmut ^{[47
]}

Hall, Alistair S. ^{[48
]}

Jarvelin, Marjo-Riitta ^{[34
,35
,49
,51
]}

Kallela, Mikko ^{[42
]}

Kaprio, Jaakko ^{[22
,23
,24
,50
]}

Kathiresan, Sekar ^{[9
,13
,14
,17
,18
]}

Lehtimaki, Terho ^{[52
,53
]}

McPherson, Ruth ^{[54
,55
]}

Marz, Winfried ^{[56
,57
,58
]}

Nyholt, Dale R. ^{[59
]}

O'Donnell, Christopher J. ^{[60
]}

Quaye, Lydia ^{[45
]}

Rader, Daniel J. ^{[61
,62
]}

Raitakari, Olli ^{[63
,64
]}

Roberts, Robert ^{[54
]}

Schunkert, Heribert ^{[32
,33
]}

Schurks, Markus ^{[65
]}

Stewart, Alexandre F. R. ^{[54
]}

Terwindt, Gisela M. ^{[29
]}

机构：

[1] Oslo Univ Hosp, Dept Neurol, Oslo, Norway

[2] Oslo Univ Hosp, FORMI, Oslo, Norway

[3] Univ Oslo, Inst Clin Med, Oslo, Norway

[4] Wellcome Trust Genome Campus, Wellcome Trust Sanger Inst, Cambridge, England

[5] Univ Leicester, Dept Cardiovasc Sci, Leicester, Leics, England

[6] Glenfield Hosp, Clin Sci Wing & Natl Inst Hlth Res Leicester, Biomed Res Unit Cardiovasc Dis, Leicester, Leics, England

[7] Ludwig Maximilians Univ Munchen, Klinikum Univ Munchen, Inst Stroke & Dementia Res, Munich, Germany

[8] Munich Cluster Syst Neurol SyNergy, Munich, Germany

[9] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA

[10] Broad Inst, Stanley Ctr Psychiat Res, Cambridge, MA USA

[11] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA

[12] Massachusetts Gen Hosp, Dept Psychiat, Analyt & Translat Genet Unit, Boston, MA 02114 USA

[13] Massachusetts Gen Hosp, Dept Med, Ctr Human Genet Res, Boston, MA 02114 USA

[14] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA

[15] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA

[16] Harvard Med Sch, Div Prevent Med, Boston, MA USA

[17] Harvard Med Sch, Brigham & Womens Hosp, Boston, MA USA

[18] Harvard Med Sch, Dept Med, Boston, MA USA

[19] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA

[20] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA

[21] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England

[22] Univ Helsinki, Dept Publ Hlth, Helsinki, Finland

[23] Univ Helsinki, Hjelt Inst, Helsinki, Finland

[24] Univ Helsinki, Inst Mol Med Finland, Helsinki, Finland

[25] Erasmus Univ, Med Ctr, Dept Epidemiol, Rotterdam, Netherlands

[26] Erasmus Univ, Med Ctr, Dept Radiol, Rotterdam, Netherlands

[27] Erasmus Univ, Med Ctr, Dept Neurol, Rotterdam, Netherlands

[28] Leiden Univ, Med Ctr, Dept Human Genet, Leiden, Netherlands

[29] Leiden Univ, Med Ctr, Dept Neurol, Leiden, Netherlands

[30] Univ Tubingen, Dept Neurol & Epileptol, Tubingen, Germany

[31] Univ Tubingen, Hertie Inst Clin Brain Res, Tubingen, Germany

[32] Tech Univ Munich, Deutsch Herzzentrum Munchen, Munich, Germany

[33] DZHK German Ctr Cardiovasc Res, Partner Site Munich Heart Alliance, Munich, Germany

[34] Univ Oulu, Inst Hlth Sci, Oulu, Finland

[35] Univ Oulu, Bioctr Oulu, Oulu, Finland

[36] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands

[37] Vrije Univ Amsterdam, Med Ctr, EMGO Inst Hlth & Care Res, Amsterdam, Netherlands

[38] Univ Bristol, MRC, Bristol, Avon, England

[39] Univ Lubeck, Inst Integrat & Expt Genom, Lubeck, Germany

[40] DZHK German Res Ctr Cardiovasc Res, Partner Site Hamburg Lubeck Kiel, Lubeck, Germany

[41] Univ Copenhagen, Dept Neurol, Glostrup Hosp, Copenhagen, Denmark

[42] Univ Helsinki, Cent Hosp, Dept Neurol, Helsinki, Finland

[43] Stanford Univ, Sch Med, Dept Med, Stanford, CA USA

[44] Johannes Gutenberg Univ Mainz, Univ Med Mainz, Med Klin & Poliklin, Mainz, Germany

[45] Kings Coll London, Dept Twin Res & Genet Epidemiol, London, England

[46] Washington Hosp Ctr, MedStar Heart Inst, Washington, DC 20010 USA

[47] Kiel Pain & Headache Ctr, Kiel, Germany

[48] Univ Leeds, Leeds Inst Genet Hlth & Therapeut, Multidisciplinary Cardiovasc Res Ctr, Div Cardiovasc & Neuronal Remodelling, Leeds, W Yorkshire, England

[49] Natl Inst Hlth & Welf, Dept Children Young People & Families, Helsinki, Finland

[50] Natl Inst Hlth & Welf, Dept Mental Hlth & Substance Abuse Serv, Helsinki, Finland

来源：

NEUROLOGY-GENETICS | 2015年 / 1卷 / 01期

基金：

英国医学研究理事会; 英国惠康基金; 芬兰科学院;

关键词：

D O I：

10.1212/NXG.0000000000000010

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Objective: To apply genetic analysis of genome-wide association data to study the extent and nature of a shared biological basis between migraine and coronary artery disease (CAD). Methods: Four separate methods for cross-phenotype genetic analysis were applied on data from 2 large-scale genome-wide association studies of migraine (19,981 cases, 56,667 controls) and CAD (21,076 cases, 63,014 controls). The first 2 methods quantified the extent of overlapping risk variants and assessed the load of CAD risk loci in migraineurs. Genomic regions of shared risk were then identified by analysis of covariance patterns between the 2 phenotypes and by querying known genome-wide significant loci. Results: We found a significant overlap of genetic risk loci for migraine and CAD. When stratified by migraine subtype, this was limited to migraine without aura, and the overlap was protective in that patients with migraine had a lower load of CAD risk alleles than controls. Genes indicated by 16 shared risk loci point to mechanisms with potential roles in migraine pathogenesis and CAD, including endothelial dysfunction (PHACTR1) and insulin homeostasis (GIP). Conclusions: The results suggest that shared biological processes contribute to risk of migraine and CAD, but surprisingly this commonality is restricted to migraine without aura and the impact is in opposite directions. Understanding the mechanisms underlying these processes and their opposite relationship to migraine and CAD may improve our understanding of both disorders.

引用

页数：10

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