Replication of a genome-wide association study of panic disorder in a Japanese population

被引:32
作者
Otowa, Takeshi [1 ]
Tanii, Hisashi [2 ]
Sugaya, Nagisa [3 ]
Yoshida, Eiji [3 ]
Inoue, Ken [4 ]
Yasuda, Shin [3 ]
Shimada, Takafumi
Kawamura, Yoshiya
Tochigi, Mamoru
Minato, Takanobu
Umekage, Tadashi
Miyagawa, Taku [5 ]
Nishida, Nao [5 ]
Tokunaga, Katsushi [5 ]
Okazaki, Yuji [6 ]
Kaiya, Hisanobu [3 ,7 ]
Sasaki, Tsukasa [8 ,9 ,10 ]
机构
[1] Univ Tokyo, Dept Neuropsychiat, Grad Sch Med, Bunkyo Ku, Tokyo 1138655, Japan
[2] Mie Univ, Grad Sch Med, Dept Neuropsychiat, Tsu, Mie, Japan
[3] Akasaka Mental Clin, Outpatient Clin Anxiety Disorders, Tokyo, Japan
[4] Fujita Hlth Univ, Sch Med, Dept Publ Hlth, Aichi, Japan
[5] Univ Tokyo, Grad Sch Med, Dept Human Genet, Tokyo 1138655, Japan
[6] Tokyo Metropolitan Matsuzawa Hosp, Dept Neurol, Tokyo, Japan
[7] Nagoya Mental Clin, Res Ctr Pan Disorder, Nagoya, Aichi, Japan
[8] Univ Tokyo, Hlth Serv Ctr, Tokyo 1138655, Japan
[9] Univ Tokyo, Off Mental Hlth Support, Tokyo 1138655, Japan
[10] Univ Tokyo, Grad Sch Educ, Tokyo 1138655, Japan
关键词
genome-wide association study (GWAS); Japanese population; panic disorder; replication; single nucleotide polymorphism (SNP); RECEPTOR GENE POLYMORPHISM; SUSCEPTIBILITY LOCUS; ANXIETY DISORDER; LINKAGE; FAMILY; SCHIZOPHRENIA; EPIDEMIOLOGY; FREQUENCY; SCREEN; POWER;
D O I
10.1038/jhg.2009.127
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Panic disorder (PD) is an anxiety disorder characterized by recurrent and unexpected panic attacks, subsequent worry and phobic avoidance. Although a number of association and linkage studies have been conducted, no gene has been identified as a susceptibility locus. We previously conducted a genome-wide association analysis of PD in 200 Japanese patients and the same number of controls, using a 500 K single nucleotide polymorphisms (SNPs) chip. In this study, we report a replication analysis of PD using the DigTag2 assay. The second stage sample consisted of 558 Japanese patients and 566 controls. Thirty-two markers were tested in a replication sample. As a result, no significant association was found after correction for multiple testing. However, the difference was observed at the nominal allele P-value <0.05 for two SNPs (rs6733840 and rs132617). We also conducted haplotype analyses of SNPs in the APOL3 and CLU genes. Our results failed to show any significant association with PD in these genes. Further studies on these variants with a larger sample size may be worth testing to confirm the results. Journal of Human Genetics (2010) 55, 91-96; doi: 10.1038/jhg.2009.127; published online 4 December 2009
引用
收藏
页码:91 / 96
页数:6
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