Please cite this article as follows: Netzer C, Freudenberg J, Toliat MR, Heinze A, Heinze-Kuhn K, Thiele H, Goebel I, Nürnberg P, Ptáček LJ, Göbel H, Todt U, Kubisch C. 2007. Genetic Association Studies of the Chromosome 15 GABA-A Receptor Cluster in Migraine With Aura. Am J Med Genet Part B 147B:37–41.
Genetic association studies of the chromosome 15 GABA-A receptor cluster in migraine with aura†
Article first published online: 6 AUG 2007
Copyright © 2007 Wiley-Liss, Inc.
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume 147B, Issue 1, pages 37–41, 5 January 2008
How to Cite
Netzer, C., Freudenberg, J., Toliat, M. R., Heinze, A., Heinze-Kuhn, K., Thiele, H., Goebel, I., Nürnberg, P., Ptáček, L. J., Göbel, H., Todt, U. and Kubisch, C. (2008), Genetic association studies of the chromosome 15 GABA-A receptor cluster in migraine with aura. Am. J. Med. Genet., 147B: 37–41. doi: 10.1002/ajmg.b.30560
- Issue published online: 14 DEC 2007
- Article first published online: 6 AUG 2007
- Manuscript Accepted: 3 APR 2007
- Manuscript Received: 14 AUG 2006
- Deutsche Forschungsgemeinschaft (DFG). Grant Numbers: FOR 423, TPA2
- National Genome Network (NGFN) by the Bundesministerium für Bildung und Forschung (BMBF). Grant Numbers: FKZ-01GS0115, FKZ-01GR0416
- GABA-A receptor;
- association study
Recently, a novel susceptibility locus for migraine with aura (MA) on chromosome 15q containing three GABA-A receptor subunits has been identified by linkage analysis in several large pedigrees. To further study the role of this locus in MA etiology we genotyped 56 SNPs capturing the known common haplotype variations of these three candidate genes in a sample comprising 270 MA patients and 273 matched controls. In a single marker analysis, four SNPs displayed nominally significant (P < 0.05) association with MA. However, after permutation-based correction for the number of tests performed, the P-values of these SNPs were non-significant. Furthermore, a replication study of two of these SNPs in a second independent sample of 379 MA patients and 379 controls did not result in a significant finding. We also compared haplotype estimates based on case–control genotypes. Again we could not demonstrate a significant association with the phenotype after correction for multiple testing. In summary, we found no convincing evidence for an involvement of common SNPs at the GABA-A receptor cluster on 15q11-q12 in the pathophysiology of MA. © 2007 Wiley-Liss, Inc.