Genome-wide association analysis of gender differences in major depressive disorder in the Netherlands NESDA and NTR population-based samples

被引:43
作者
Aragam, Nagesh [1 ]
Wang, Ke-Sheng [1 ]
Pan, Yue [2 ]
机构
[1] E Tennessee State Univ, Coll Publ Hlth, Dept Biostat & Epidemiol, Johnson City, TN 37614 USA
[2] E Tennessee State Univ, Coll Arts & Sci, Dept Math & Stat, Johnson City, TN 37614 USA
基金
美国国家卫生研究院;
关键词
Major depressive disorder; Gender difference; Genome-wide association; FIGN; LGSN; PCLO; ODOR RECOGNITION; PROTEIN PICCOLO; MOLECULAR-BASIS; PCLO GENE; FAMILY; POLYMORPHISM; REPLICATION; COMORBIDITY; PREVALENCE; LENGSIN;
D O I
10.1016/j.jad.2011.04.054
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Major depressive disorder (MDD) is a universally prevalent, genetic, and environment dependent mental condition that disables people of every culture, race, gender, and age. While the gender differences for MDD have been widely reported in literature, few genome-wide analyses of gender differences have been reported to date. Methods: We conducted a genome-wide association analysis of gender differences for MDD using the Netherlands NESDA and NTR population-based samples (1726 cases and 1630 controls). PLINK software was used to analyze the genome-wide association data of Perlegen 600 K SNP Chips. Results: We identified 40 male-specific and 56 female-specific MDD associated SNPs with P-values less than 10(-4). The best male-specific SNP was rs9352774 (P= 2.26 x 10(-6)) within LGSN gene while the best female-specific SNP was rs2715148 (P= 5.64 x 10(-7)) within PCLO gene. We also found 38 SNPs showing gene x gender interactions in influencing MDD (P<10(-4)). The best SNP was rs12692709 (P = 5.75 x 10(-6)) near FIGN gene at 2q24.3 while the next best SNP was rs11039588 (P.= 1.16x 10(-5)) within OR4B1 gene. Limitations: The findings from this study need be replicated in other populations. Conclusions: These results provide genetic basis for gender differences in MDD and will serve as a resource for replication in other populations to elucidate the potential role of these genetic variants in MDD. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:516 / 521
页数:6
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