期刊
NATURE GENETICS
卷 43, 期 10, 页码 977-U162出版社
NATURE PORTFOLIO
DOI: 10.1038/ng.943
关键词
-
资金
- US National Institutes of Health (NIH) [MH078151, MH081804, MH059567, MH59553, MH080372, 1U54RR025204]
- Genetic Association Information Network (GAIN)
- NIMH Intramural Research Program
- Tzedakah Foundation
- American Philosophical Society
- Stardust foundation
- National Library of Medicine
- Stanley Foundation for Medical Research
- Wellcome Trust
- Pritzker Neuropsychiatric Disorders Research Fund L.L.C.
- GlaxoSmithKline
- Research Council of Norway [167153/V50, 163070/V50, 175345/V50]
- South-East Norway Health Authority [123-2004]
- EU (ENBREC)
- MRC [G1000718, G1000708, G0701007, G0701003] Funding Source: UKRI
- Medical Research Council [G0701007, G9817803B, G0701003, G1000708, G1000718, G0801418B] Funding Source: researchfish
We conducted a combined genome-wide association study (GWAS) of 7,481 individuals with bipolar disorder (cases) and 9,250 controls as part of the Psychiatric GWAS Consortium. Our replication study tested 34 SNPs in 4,496 independent cases with bipolar disorder and 42,422 independent controls and found that 18 of 34 SNPs had P < 0.05, with 31 of 34 SNPs having signals with the same direction of effect (P = 3.8 x 10(-7)). An analysis of all 11,974 bipolar disorder cases and 51,792 controls confirmed genome-wide significant evidence of association for CACNA1C and identified a new intronic variant in ODZ4. We identified a pathway comprised of subunits of calcium channels enriched in bipolar disorder association intervals. Finally, a combined GWAS analysis of schizophrenia and bipolar disorder yielded strong association evidence for SNPs in CACNA1C and in the region of NEK4-ITIH1-ITIH3-ITIH4. Our replication results imply that increasing sample sizes in bipolar disorder will confirm many additional loci.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据