A genome-wide association study identifies two novel susceptibility loci and trans population polygenicity associated with bipolar disorder
Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887...
Saved in:
Published in | Molecular psychiatry Vol. 23; no. 3; pp. 639 - 647 |
---|---|
Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.03.2018
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456,
P
=6.4 × 10
−9
), a region known to contain regulatory genes for plasma lipid levels (
FADS1/2/3
). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene,
NFIX
(
P
best
=5.8 × 10
−10
), and supported three regions previously implicated in BD susceptibility:
MAD1L1
(
P
best
=1.9 × 10
−9
),
TRANK1
(
P
best
=2.1 × 10
−9
) and
ODZ4
(
P
best
=3.3 × 10
−9
). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or
vice versa
(for ‘within Japanese comparisons’,
P
best
~10
−29
,
R
2
~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for ‘trans-European-Japanese comparison,’
P
best
~10
−13
,
R
2
~0.27%). This ‘trans population’ effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD ‘risk’ effect are shared between Japanese and European populations. |
---|---|
AbstractList | Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P=6.4 x 10[sup.-9]), a region known to contain regulatory genes for plasma lipid levels (FADS1/2/3). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (P[sub.best]=5.8 x 10[sup.-10]), and supported three regions previously implicated in BD susceptibility: MAD1L1 (P[sub.best]=1.9 x 10[sup.-9]), TRANK1 (P[sub.best]=2.1 x 10[sup.-9]) and ODZ4 (P[sub.best]=3.3 x 10[sup.-9]). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for 'within Japanese comparisons', P[sub.best]~10[sup.-29], R[sup.2]~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for 'trans-European-Japanese comparison,' P[sub.best]~10[sup.-13], R[sup.2]~0.27%). This 'trans population' effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD 'risk' effect are shared between Japanese and European populations. Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P =6.4 × 10 −9 ), a region known to contain regulatory genes for plasma lipid levels ( FADS1/2/3 ). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX ( P best =5.8 × 10 −10 ), and supported three regions previously implicated in BD susceptibility: MAD1L1 ( P best =1.9 × 10 −9 ), TRANK1 ( P best =2.1 × 10 −9 ) and ODZ4 ( P best =3.3 × 10 −9 ). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for ‘within Japanese comparisons’, P best ~10 −29 , R 2 ~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for ‘trans-European-Japanese comparison,’ P best ~10 −13 , R 2 ~0.27%). This ‘trans population’ effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD ‘risk’ effect are shared between Japanese and European populations. Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P=6.4 × 10-9), a region known to contain regulatory genes for plasma lipid levels (FADS1/2/3). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (Pbest=5.8 × 10-10), and supported three regions previously implicated in BD susceptibility: MAD1L1 (Pbest=1.9 × 10-9), TRANK1 (Pbest=2.1 × 10-9) and ODZ4 (Pbest=3.3 × 10-9). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for 'within Japanese comparisons', Pbest~10-29, R2~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for 'trans-European-Japanese comparison,' Pbest~10-13, R2~0.27%). This 'trans population' effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD 'risk' effect are shared between Japanese and European populations.Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P=6.4 × 10-9), a region known to contain regulatory genes for plasma lipid levels (FADS1/2/3). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (Pbest=5.8 × 10-10), and supported three regions previously implicated in BD susceptibility: MAD1L1 (Pbest=1.9 × 10-9), TRANK1 (Pbest=2.1 × 10-9) and ODZ4 (Pbest=3.3 × 10-9). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for 'within Japanese comparisons', Pbest~10-29, R2~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for 'trans-European-Japanese comparison,' Pbest~10-13, R2~0.27%). This 'trans population' effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD 'risk' effect are shared between Japanese and European populations. Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P=6.4 × 10 ), a region known to contain regulatory genes for plasma lipid levels (FADS1/2/3). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (P =5.8 × 10 ), and supported three regions previously implicated in BD susceptibility: MAD1L1 (P =1.9 × 10 ), TRANK1 (P =2.1 × 10 ) and ODZ4 (P =3.3 × 10 ). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for 'within Japanese comparisons', P ~10 , R ~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for 'trans-European-Japanese comparison,' P ~10 , R ~0.27%). This 'trans population' effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD 'risk' effect are shared between Japanese and European populations. Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P=6.4 x 10[sup.-9]), a region known to contain regulatory genes for plasma lipid levels (FADS1/2/3). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (P[sub.best]=5.8 x 10[sup.-10]), and supported three regions previously implicated in BD susceptibility: MAD1L1 (P[sub.best]=1.9 x 10[sup.-9]), TRANK1 (P[sub.best]=2.1 x 10[sup.-9]) and ODZ4 (P[sub.best]=3.3 x 10[sup.-9]). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for 'within Japanese comparisons', P[sub.best]~10[sup.-29], R[sup.2]~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for 'trans-European-Japanese comparison,' P[sub.best]~10[sup.-13], R[sup.2]~0.27%). This 'trans population' effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD 'risk' effect are shared between Japanese and European populations. Molecular Psychiatry (2018) 23, 639-647; doi: 10.1038/mp.2016.259; published online 24 January 2017 Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P=6.4 × 10-9 ), a region known to contain regulatory genes for plasma lipid levels (FADS1/2/3). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (Pbest =5.8 × 10-10 ), and supported three regions previously implicated in BD susceptibility: MAD1L1 (Pbest =1.9 × 10-9 ), TRANK1 (Pbest =2.1 × 10-9 ) and ODZ4 (Pbest =3.3 × 10-9 ). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for 'within Japanese comparisons', Pbest ~10-29 , R2 ~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for 'trans-European-Japanese comparison,' Pbest ~10-13 , R2 ~0.27%). This 'trans population' effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD 'risk' effect are shared between Japanese and European populations. |
Audience | Academic |
Author | Kato, T Kitajima, T Takahashi, A Ozaki, N Iwata, N Yoneda, H Someya, T Hashimoto, R Ikeda, M Sasaki, T Ohmori, T Yoshikawa, T Inada, T Kubo, M Kamatani, Y Kawasaki, H Kashiwase, K Matsuda, K Yoshimura, R Shimodera, S Akiyama, K Akiyama, M Tanii, H Mori, N Shimasaki, A Itokawa, M Kunugi, H Kawase, K Saito, T Inoue, T Matsuo, K Kanba, S Ashikawa, K Iyo, M Tokunaga, K Kondo, K Kusumi, I Okahisa, Y Okamoto, Y Arai, H |
Author_xml | – sequence: 1 givenname: M surname: Ikeda fullname: Ikeda, M organization: Department of Psychiatry, Fujita Health University School of Medicine – sequence: 2 givenname: A surname: Takahashi fullname: Takahashi, A organization: Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Laboratory for Omics Informatics, Omics Research Center, National Cerebral and Cardiovascular Center – sequence: 3 givenname: Y surname: Kamatani fullname: Kamatani, Y organization: Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences – sequence: 4 givenname: Y surname: Okahisa fullname: Okahisa, Y organization: Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences – sequence: 5 givenname: H surname: Kunugi fullname: Kunugi, H organization: Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry – sequence: 6 givenname: N surname: Mori fullname: Mori, N organization: Department of Psychiatry and Neurology, Hamamatsu University School of Medicine – sequence: 7 givenname: T surname: Sasaki fullname: Sasaki, T organization: Laboratory of Health Education, Graduate School of Education, the University of Tokyo – sequence: 8 givenname: T surname: Ohmori fullname: Ohmori, T organization: Department of Psychiatry, Course of Integrated Brain Sciences, Medical Informatics, Institute of Health Biosciences, The University of Tokushima Graduate School – sequence: 9 givenname: Y surname: Okamoto fullname: Okamoto, Y organization: Department of Psychiatry and Neurosciences, Graduate School of Biomedical and Health Sciences, Hiroshima University – sequence: 10 givenname: H surname: Kawasaki fullname: Kawasaki, H organization: Department of Psychiatry, Fukuoka University, Faculty of Medicine – sequence: 11 givenname: S surname: Shimodera fullname: Shimodera, S organization: Department of Neuropsychiatry, Kochi Medical School, Kochi University – sequence: 12 givenname: T surname: Kato fullname: Kato, T organization: Laboratory for Molecular Dynamics of Mental Disorders, RIKEN Brain Science Institute – sequence: 13 givenname: H surname: Yoneda fullname: Yoneda, H organization: Department of Neuropsychiatry, Osaka Medical College – sequence: 14 givenname: R surname: Yoshimura fullname: Yoshimura, R organization: Department of Psychiatry, University of Occupational and Environmental Health – sequence: 15 givenname: M surname: Iyo fullname: Iyo, M organization: Department of Psychiatry, Chiba University Graduate School of Medicine – sequence: 16 givenname: K surname: Matsuda fullname: Matsuda, K organization: Laboratory of Clinical Sequence, Graduate School of Frontier Sciences, The University of Tokyo – sequence: 17 givenname: M surname: Akiyama fullname: Akiyama, M organization: Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences – sequence: 18 givenname: K surname: Ashikawa fullname: Ashikawa, K organization: Laboratory for Genotyping Development, Center for Integrative Medical Sciences, RIKEN – sequence: 19 givenname: K surname: Kashiwase fullname: Kashiwase, K organization: Japanese Red Cross Kanto-Koshinetsu Block Blood Center – sequence: 20 givenname: K surname: Tokunaga fullname: Tokunaga, K organization: Department of Human Genetics, Graduate School of Medicine, University of Tokyo – sequence: 21 givenname: K surname: Kondo fullname: Kondo, K organization: Department of Psychiatry, Fujita Health University School of Medicine – sequence: 22 givenname: T surname: Saito fullname: Saito, T organization: Department of Psychiatry, Fujita Health University School of Medicine – sequence: 23 givenname: A surname: Shimasaki fullname: Shimasaki, A organization: Department of Psychiatry, Fujita Health University School of Medicine – sequence: 24 givenname: K surname: Kawase fullname: Kawase, K organization: Department of Psychiatry, Fujita Health University School of Medicine – sequence: 25 givenname: T surname: Kitajima fullname: Kitajima, T organization: Department of Psychiatry, Fujita Health University School of Medicine – sequence: 26 givenname: K surname: Matsuo fullname: Matsuo, K organization: Division of Neuropsychiatry, Department of Neuroscience, Yamaguchi University Graduate School of Medicine – sequence: 27 givenname: M surname: Itokawa fullname: Itokawa, M organization: Center for Medical Cooperation, Tokyo Metropolitan Institute of Medical Science – sequence: 28 givenname: T surname: Someya fullname: Someya, T organization: Department of Psychiatry, Niigata University Graduate School of Medical and Dental Sciences – sequence: 29 givenname: T surname: Inada fullname: Inada, T organization: Department of Psychiatry, Nagoya University, Graduate School of Medicine – sequence: 30 givenname: R surname: Hashimoto fullname: Hashimoto, R organization: Molecular Research Center for Children's Mental Development, United Graduate School of Child Development, Osaka University – sequence: 31 givenname: T surname: Inoue fullname: Inoue, T organization: Department of Psychiatry, Tokyo Medical University – sequence: 32 givenname: K surname: Akiyama fullname: Akiyama, K organization: Department of Biological Psychiatry and Neuroscience, Dokkyo Medical University School of Medicine – sequence: 33 givenname: H surname: Tanii fullname: Tanii, H organization: Department of Neuropsychiatry, Mie University, Graduate School of Medicine – sequence: 34 givenname: H surname: Arai fullname: Arai, H organization: Department of Psychiatry and Behavioral Sciences, Juntendo Graduate School of Medicine – sequence: 35 givenname: S surname: Kanba fullname: Kanba, S organization: Department of Neuropsychiatry, Kyushu University, Graduate School of Medical Sciences – sequence: 36 givenname: N surname: Ozaki fullname: Ozaki, N organization: Department of Psychiatry, Nagoya University, Graduate School of Medicine – sequence: 37 givenname: I surname: Kusumi fullname: Kusumi, I organization: Department of Psychiatry, Hokkaido University Graduate School of Medicine – sequence: 38 givenname: T surname: Yoshikawa fullname: Yoshikawa, T organization: Laboratory for Molecular Psychiatry, RIKEN Brain Science Institute – sequence: 39 givenname: M surname: Kubo fullname: Kubo, M organization: RIKEN Center for Integrative Medical Sciences – sequence: 40 givenname: N surname: Iwata fullname: Iwata, N email: nakao@fujita-hu.ac.jp organization: Department of Psychiatry, Fujita Health University School of Medicine |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28115744$$D View this record in MEDLINE/PubMed |
BookMark | eNp1kktr3DAUhUVJaR7tqvsi6KaQeirZkkazCQyhLwh0066FLEsTBVlyJTvD_Ib-6V5n8mhCihYW93732MfnHqODmKJF6C0lC0oa-akfFjWhYlHz1Qt0RNlSVJwv5QHcG76qGJXsEB2XckXI3OSv0GEtKeVLxo7QnzXe2Jh6W219Z7EuJRmvR58iLuPU7TBU4-idtwWP24RjurYBl6kYO4y-9cGPOxxgBuvY4THrWPCQhinsNYYUdqDvzYzdidsOb_14iVsPbZ1x50vKnc2v0UunQ7Fvbp8n6NeXzz_Pv1UXP75-P19fVEbUzVg5QgwjjhHhRC3dikvihNNN45whRi-b1grZutZyo52UjLKu1quOMWacYACeoLO97jC1ve0MGMw6qCH7XuedStqrx53oL9UmXSsu65oxCQIfbgVy-j3ZMqreww8JQUebpqKoFFQQQRkD9P0T9CpNOYI9VRPCCKMrJh6ojQ5W-egSvNfMomrNISxJIVGgFs9QcDrbewNL4TzUHw28-9fovcO7-AE43QMmp1KydfcIJWpeLtUPal4uBcsFNH1CQ6w3OcN3-PCfmY_7mQLKcWPzg__n8L_EpOPz |
CitedBy_id | crossref_primary_10_3389_fgene_2021_535123 crossref_primary_10_1017_S0033291721001252 crossref_primary_10_1038_s41398_018_0337_x crossref_primary_10_1007_s00439_021_02299_8 crossref_primary_10_1016_j_jad_2024_10_063 crossref_primary_10_1038_s41380_020_0782_9 crossref_primary_10_1038_s41598_021_84739_z crossref_primary_10_1159_000539115 crossref_primary_10_1002_jnr_24609 crossref_primary_10_1001_jamapsychiatry_2020_3738 crossref_primary_10_1371_journal_pgen_1009733 crossref_primary_10_3389_fpsyt_2019_00312 crossref_primary_10_1159_000488590 crossref_primary_10_1038_s41398_024_03141_1 crossref_primary_10_1007_s00439_019_02096_4 crossref_primary_10_1111_pcn_13311 crossref_primary_10_1186_s12864_023_09425_y crossref_primary_10_1002_npr2_12409 crossref_primary_10_1038_s41380_023_01988_2 crossref_primary_10_1038_s41380_023_02096_x crossref_primary_10_1016_j_pbiomolbio_2024_11_002 crossref_primary_10_1093_schbul_sbab023 crossref_primary_10_1111_jcmm_16611 crossref_primary_10_1002_pcn5_70071 crossref_primary_10_3390_ijms241411777 crossref_primary_10_1038_s41386_020_00788_4 crossref_primary_10_1096_fj_201901598R crossref_primary_10_1038_s41380_018_0332_x crossref_primary_10_1038_s41467_020_20443_2 crossref_primary_10_1038_s41586_024_08468_9 crossref_primary_10_1080_00207454_2023_2251661 crossref_primary_10_3390_genes13081303 crossref_primary_10_4306_jknpa_2018_57_4_276 crossref_primary_10_3390_brainsci7100134 crossref_primary_10_3389_fmars_2021_742330 crossref_primary_10_3390_biom15030383 crossref_primary_10_7717_peerj_7778 crossref_primary_10_1038_s41398_025_03287_6 crossref_primary_10_1038_s41398_019_0548_9 crossref_primary_10_1073_pnas_2005753118 crossref_primary_10_1186_s41065_019_0095_7 crossref_primary_10_1038_s41398_022_01959_1 crossref_primary_10_1097_YPG_0000000000000304 crossref_primary_10_3390_nu12020356 crossref_primary_10_1038_s41398_022_01802_7 crossref_primary_10_2298_ABS240904029P crossref_primary_10_1038_s41588_021_00857_4 crossref_primary_10_14789_jmj_JMJ21_0026_R crossref_primary_10_1038_s41467_021_23453_w crossref_primary_10_1038_s41398_019_0536_0 crossref_primary_10_1038_s42003_022_03972_y crossref_primary_10_1097_YPG_0000000000000272 crossref_primary_10_1016_j_biopsych_2024_02_1005 crossref_primary_10_1016_j_bbalip_2024_159564 crossref_primary_10_1111_pcn_13498 crossref_primary_10_1192_bjo_2021_1082 crossref_primary_10_3389_fgene_2019_00258 crossref_primary_10_1016_j_neuron_2022_09_028 crossref_primary_10_1038_s41386_020_0605_3 crossref_primary_10_1016_j_pnpbp_2025_111298 crossref_primary_10_1038_s41398_017_0019_0 crossref_primary_10_1002_hbm_25040 crossref_primary_10_1186_s13148_022_01394_5 crossref_primary_10_61373_gp024i_0049 crossref_primary_10_3390_cells11010172 crossref_primary_10_1038_s41398_020_0777_y crossref_primary_10_1038_s41398_019_0407_8 crossref_primary_10_1016_j_pnpbp_2020_110227 crossref_primary_10_1152_ajpendo_00331_2024 crossref_primary_10_1093_cercor_bhad059 crossref_primary_10_1038_s41380_024_02718_y crossref_primary_10_1007_s00125_022_05665_x crossref_primary_10_1186_s12864_023_09434_x crossref_primary_10_3389_fgene_2023_1191264 crossref_primary_10_1016_j_ajhg_2022_04_004 crossref_primary_10_1017_S0033291718000685 crossref_primary_10_1038_s10038_020_0814_y crossref_primary_10_1038_s41380_023_02087_y crossref_primary_10_1038_s42003_020_01383_5 crossref_primary_10_1016_j_nsa_2024_104087 crossref_primary_10_1016_j_biopsych_2017_09_010 crossref_primary_10_1186_s12967_022_03637_8 crossref_primary_10_1038_s41380_019_0634_7 crossref_primary_10_1007_s11920_019_1123_z crossref_primary_10_1038_s41386_019_0506_5 crossref_primary_10_1016_j_bpsgos_2023_07_004 crossref_primary_10_1186_s13059_023_03068_8 crossref_primary_10_1016_j_neubiorev_2023_105476 crossref_primary_10_1111_pcn_13752 crossref_primary_10_1080_00401706_2023_2257760 crossref_primary_10_1038_s41380_025_02934_0 crossref_primary_10_3389_fcell_2022_956265 crossref_primary_10_3389_fnmol_2019_00035 crossref_primary_10_1097_YPG_0000000000000302 crossref_primary_10_3390_ijms26052368 crossref_primary_10_1038_s41380_021_01274_z crossref_primary_10_1038_s41588_019_0397_8 crossref_primary_10_14789_jmj_JMJ21_0038_R crossref_primary_10_1016_j_isci_2021_103063 crossref_primary_10_1080_14737175_2019_1550361 crossref_primary_10_1002_alz_70031 crossref_primary_10_1016_j_biopsych_2023_01_027 crossref_primary_10_1186_s12889_023_16764_8 crossref_primary_10_1038_s41588_018_0047_6 crossref_primary_10_1038_s41398_019_0488_4 crossref_primary_10_1186_s13073_022_01057_3 crossref_primary_10_1016_j_jmb_2018_05_037 crossref_primary_10_1016_j_bbrep_2019_100660 crossref_primary_10_1016_j_biopsych_2019_10_015 crossref_primary_10_1016_j_pnpbp_2018_08_035 crossref_primary_10_1016_j_psychres_2021_113880 crossref_primary_10_1001_jamapsychiatry_2020_3639 crossref_primary_10_1038_s41380_022_01856_5 crossref_primary_10_1016_j_biopsych_2019_10_011 crossref_primary_10_1038_s41398_019_0383_z crossref_primary_10_1080_09291016_2018_1465249 crossref_primary_10_1016_j_tcb_2018_09_003 crossref_primary_10_3389_fpsyt_2024_1414776 crossref_primary_10_1186_s12967_024_05053_6 crossref_primary_10_3389_fgene_2021_789512 crossref_primary_10_1038_s10038_022_01046_9 crossref_primary_10_1038_s41380_024_02663_w crossref_primary_10_1016_j_jpsychires_2022_09_038 crossref_primary_10_1111_pcn_12926 crossref_primary_10_3390_metabo13090981 crossref_primary_10_1038_s41398_019_0561_z crossref_primary_10_1007_s12264_023_01169_9 crossref_primary_10_1038_s41380_018_0314_z crossref_primary_10_1093_schbul_sby140 |
Cites_doi | 10.1038/nature13595 10.1016/j.tig.2008.12.002 10.1038/ng.2742 10.1038/ng.943 10.1016/j.jad.2013.02.019 10.2174/1573409910666140410124315 10.1038/ng.3211 10.1038/nature09534 10.1016/j.ajhg.2011.01.017 10.1038/ncomms4339 10.1007/s12291-012-0292-x 10.1002/ajmg.b.30941 10.1093/bioinformatics/btq419 10.1016/S0378-1119(00)00140-2 10.1038/mp.2011.157 10.1038/nature08185 10.1007/s12263-015-0502-2 10.1016/j.genhosppsych.2015.04.003 10.1038/ng.2797 10.1038/ng.2711 10.1093/bioinformatics/btu848 10.1016/S0140-6736(13)60855-7 10.1038/mp.2013.138 10.1016/j.ajhg.2016.05.001 10.1371/journal.pgen.1002193 10.1161/CIRCGENETICS.113.000208 10.1038/mp.2012.142 10.1038/mp.2010.43 10.1038/ng.3404 10.1016/j.jad.2010.04.012 10.1016/j.schres.2015.03.034 10.1016/j.biopsych.2010.07.010 |
ContentType | Journal Article |
Copyright | The Author(s) 2018 COPYRIGHT 2018 Nature Publishing Group Copyright Nature Publishing Group Mar 2018 Copyright © 2018 The Author(s) 2018 The Author(s) |
Copyright_xml | – notice: The Author(s) 2018 – notice: COPYRIGHT 2018 Nature Publishing Group – notice: Copyright Nature Publishing Group Mar 2018 – notice: Copyright © 2018 The Author(s) 2018 The Author(s) |
CorporateAuthor | for the advanced Collaborative Study of Mood Disorder (COSMO) team |
CorporateAuthor_xml | – name: for the advanced Collaborative Study of Mood Disorder (COSMO) team |
DBID | C6C AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7TK 7X7 7XB 88E 88G 8AO 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FYUFA GHDGH GNUQQ HCIFZ K9. LK8 M0S M1P M2M M7P PHGZM PHGZT PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS PSYQQ Q9U 7X8 5PM |
DOI | 10.1038/mp.2016.259 |
DatabaseName | Springer Nature OA Free Journals CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Neurosciences Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Psychology Database (Alumni) ProQuest Pharma Collection ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central Natural Science Collection ProQuest One Community College ProQuest Central Korea Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Biological Sciences ProQuest Health & Medical Collection Medical Database Psychology Database Biological Science Database ProQuest Central Premium ProQuest One Academic ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China ProQuest One Psychology ProQuest Central Basic MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) ProQuest One Psychology ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Biological Science Collection ProQuest Central Basic ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest Psychology Journals (Alumni) Biological Science Database ProQuest SciTech Collection Neurosciences Abstracts ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest Psychology Journals ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
DatabaseTitleList | MEDLINE - Academic MEDLINE ProQuest One Psychology |
Database_xml | – sequence: 1 dbid: C6C name: Springer Nature OA Free Journals url: http://www.springeropen.com/ sourceTypes: Publisher – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 4 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine Biology |
DocumentTitleAlternate | GWAS of bipolar disorder |
EISSN | 1476-5578 |
EndPage | 647 |
ExternalDocumentID | PMC5822448 A528181557 28115744 10_1038_mp_2016_259 |
Genre | Clinical Trial, Phase II Clinical Trial, Phase I Research Support, Non-U.S. Gov't Journal Article |
GeographicLocations | Japan |
GeographicLocations_xml | – name: Japan |
GroupedDBID | --- -Q- 0R~ 123 29M 2WC 36B 39C 3V. 4.4 406 53G 70F 7X7 88E 8AO 8FI 8FJ 8R4 8R5 AACDK AANZL AASML AATNV AAYZH AAZLF ABAKF ABAWZ ABDBF ABIVO ABJNI ABLJU ABUWG ABZZP ACAOD ACGFS ACKTT ACPRK ACRQY ACUHS ACZOJ ADBBV ADHDB AEFQL AEJRE AEMSY AENEX AEVLU AEXYK AFBBN AFKRA AFRAH AFSHS AGAYW AGHAI AGQEE AHMBA AHSBF AIGIU AILAN AJRNO ALFFA ALIPV ALMA_UNASSIGNED_HOLDINGS AMYLF AXYYD AZQEC B0M BAWUL BBNVY BENPR BHPHI BKKNO BPHCQ BVXVI C6C CAG CCPQU COF CS3 DIK DNIVK DPUIP DU5 DWQXO E3Z EAD EAP EBC EBD EBLON EBS EE. EIOEI EJD EMB EMK EMOBN EPL EPS ESX F5P FDQFY FEDTE FERAY FIGPU FIZPM FSGXE FYUFA GNUQQ HCIFZ HMCUK HVGLF HZ~ IAO IHR INH INR IPY ITC IWAJR JSO JZLTJ KQ8 M1P M2M M7P NAO NQJWS O9- OK1 OVD P2P PQQKQ PROAC PSQYO PSYQQ Q2X RNS RNT RNTTT ROL SNX SNYQT SOHCF SOJ SRMVM SV3 SWTZT TAOOD TBHMF TDRGL TEORI TR2 TSG TUS UKHRP ~8M AAYXX ABBRH ABDBE ABFSG ACSTC AEZWR AFDZB AFHIU AHWEU AIXLP ATHPR AYFIA CITATION PHGZM PHGZT ABRTQ CGR CUY CVF ECM EIF NPM PJZUB PPXIY PQGLB AEIIB PMFND 7TK 7XB 8FE 8FH 8FK K9. LK8 PKEHL PQEST PQUKI PRINS Q9U 7X8 5PM |
ID | FETCH-LOGICAL-c623t-f00c40f406f628f9580f6fa33ffc0ca73be68bfbe5caf88414d2a9d444cf64fa3 |
IEDL.DBID | C6C |
ISSN | 1359-4184 1476-5578 |
IngestDate | Thu Aug 21 14:07:55 EDT 2025 Thu Jul 10 21:56:36 EDT 2025 Sat Aug 23 13:12:23 EDT 2025 Tue Jun 17 21:17:49 EDT 2025 Tue Jun 10 20:35:22 EDT 2025 Mon Jul 21 05:41:54 EDT 2025 Thu Apr 24 23:12:53 EDT 2025 Tue Jul 01 00:21:47 EDT 2025 Fri Feb 21 02:39:28 EST 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 3 |
Language | English |
License | This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0 |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c623t-f00c40f406f628f9580f6fa33ffc0ca73be68bfbe5caf88414d2a9d444cf64fa3 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 These authors contributed equally to this work. |
OpenAccessLink | https://www.nature.com/articles/mp.2016.259 |
PMID | 28115744 |
PQID | 2004041946 |
PQPubID | 44096 |
PageCount | 9 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_5822448 proquest_miscellaneous_1861606144 proquest_journals_2004041946 gale_infotracmisc_A528181557 gale_infotracacademiconefile_A528181557 pubmed_primary_28115744 crossref_primary_10_1038_mp_2016_259 crossref_citationtrail_10_1038_mp_2016_259 springer_journals_10_1038_mp_2016_259 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2018-03-01 |
PublicationDateYYYYMMDD | 2018-03-01 |
PublicationDate_xml | – month: 03 year: 2018 text: 2018-03-01 day: 01 |
PublicationDecade | 2010 |
PublicationPlace | London |
PublicationPlace_xml | – name: London – name: England – name: New York |
PublicationTitle | Molecular psychiatry |
PublicationTitleAbbrev | Mol Psychiatry |
PublicationTitleAlternate | Mol Psychiatry |
PublicationYear | 2018 |
Publisher | Nature Publishing Group UK Nature Publishing Group |
Publisher_xml | – name: Nature Publishing Group UK – name: Nature Publishing Group |
References | Lemaitre, Tanaka, Tang, Manichaikul, Foy, Kabagambe (CR22) 2011; 7 Cichon, Muhleisen, Degenhardt, Mattheisen, Miro, Strohmaier (CR4) 2011; 88 Lee, Chen, Lee, Chen, Chong, Ouyang (CR13) 2011; 16 Muhleisen, Leber, Schulze, Strohmaier, Degenhardt, Treutlein (CR7) 2014; 5 Ruderfer, Fanous, Ripke, McQuillin, Amdur (CR31) 2014; 19 Willer, Schmidt, Sengupta, Peloso, Gustafsson (CR20) 2013; 45 Green, Hamshere, Forty, Gordon-Smith, Fraser, Russell (CR6) 2013; 18 Ripke, O'Dushlaine, Chambert, Moran, Kahler, Akterin (CR9) 2013; 45 CR33 Pruim, Welch, Sanna, Teslovich, Chines, Gliedt (CR15) 2010; 26 Hsu, Chien, Lin (CR24) 2015; 37 Finucane, Bulik-Sullivan, Gusev, Trynka, Reshef, Loh (CR17) 2015; 47 Dorajoo, Sun, Han, Ke, Burger, Chang (CR23) 2015; 10 Bulik-Sullivan, Loh, Finucane, Ripke, Yang (CR18) 2015; 47 Guha, Bhowmick, Mazumder, Ghosal, Chakraborty, Burman (CR28) 2014; 29 Lee, Ripke, Neale, Faraone, Purcell (CR11) 2013; 45 Euesden, Lewis, O’Reilly (CR16) 2015; 31 Abecasis, Altshuler, Auton, Brooks, Durbin (CR14) 2010; 467 McIntyre, Danilewitz, Liauw, Kemp, Nguyen, Kahn (CR25) 2010; 126 Craddock, Sklar (CR2) 2013; 381 Mothi, Tandon, Padmanabhan, Mathew, Clementz, Tamminga (CR27) 2015; 165 Guan, Steffen, Lemaitre, Wu, Tanaka, Manichaikul (CR21) 2014; 7 Bai, Su, Chen, Chen, Chang (CR26) 2013; 150 Purcell, Wray, Stone, Visscher, O’Donovan (CR10) 2009; 460 Brown, Ye, Price, Zaitlen (CR19) 2016; 99 Gronostajski (CR29) 2000; 249 Craddock, Sklar (CR1) 2009; 25 Chen, Jiang, Akula, Shugart, Wendland, Steele (CR5) 2013; 18 (CR8) 2014; 511 Hattori, Toyota, Ishitsuka, Iwayama, Yamada, Ujike (CR12) 2009; 150B Avram, Mernea, Mihailescu, Seiman, Seiman, Putz (CR30) 2014; 10 (CR3) 2011; 43 Ikeda, Aleksic, Kinoshita, Okochi, Kawashima, Kushima (CR32) 2011; 69 S Avram (BFmp2016259_CR30) 2014; 10 R Dorajoo (BFmp2016259_CR23) 2015; 10 BK Bulik-Sullivan (BFmp2016259_CR18) 2015; 47 HK Finucane (BFmp2016259_CR17) 2015; 47 DM Ruderfer (BFmp2016259_CR31) 2014; 19 J Euesden (BFmp2016259_CR16) 2015; 31 BFmp2016259_CR33 SM Purcell (BFmp2016259_CR10) 2009; 460 N Craddock (BFmp2016259_CR1) 2009; 25 S Ripke (BFmp2016259_CR9) 2013; 45 JH Hsu (BFmp2016259_CR24) 2015; 37 RN Lemaitre (BFmp2016259_CR22) 2011; 7 N Craddock (BFmp2016259_CR2) 2013; 381 GR Abecasis (BFmp2016259_CR14) 2010; 467 YM Bai (BFmp2016259_CR26) 2013; 150 W Guan (BFmp2016259_CR21) 2014; 7 EK Green (BFmp2016259_CR6) 2013; 18 RM Gronostajski (BFmp2016259_CR29) 2000; 249 Schizophrenia Working Group of the Psychiatric Genomics Consortium (BFmp2016259_CR8) 2014; 511 P Guha (BFmp2016259_CR28) 2014; 29 RJ Pruim (BFmp2016259_CR15) 2010; 26 Psychiatric GWAS Consortium Bipolar Disorder Working Group (BFmp2016259_CR3) 2011; 43 E Hattori (BFmp2016259_CR12) 2009; 150B CJ Willer (BFmp2016259_CR20) 2013; 45 SS Mothi (BFmp2016259_CR27) 2015; 165 BC Brown (BFmp2016259_CR19) 2016; 99 S Cichon (BFmp2016259_CR4) 2011; 88 RS McIntyre (BFmp2016259_CR25) 2010; 126 TW Muhleisen (BFmp2016259_CR7) 2014; 5 M Ikeda (BFmp2016259_CR32) 2011; 69 MT Lee (BFmp2016259_CR13) 2011; 16 DT Chen (BFmp2016259_CR5) 2013; 18 SH Lee (BFmp2016259_CR11) 2013; 45 |
References_xml | – volume: 511 start-page: 421 year: 2014 end-page: 427 ident: CR8 article-title: Biological insights from 108 schizophrenia-associated genetic loci publication-title: Nature doi: 10.1038/nature13595 – volume: 25 start-page: 99 year: 2009 end-page: 105 ident: CR1 article-title: Genetics of bipolar disorder: successful start to a long journey publication-title: Trend Genet doi: 10.1016/j.tig.2008.12.002 – volume: 45 start-page: 1150 year: 2013 end-page: 1159 ident: CR9 article-title: Genome-wide association analysis identifies 13 new risk loci for schizophrenia publication-title: Nat Genet doi: 10.1038/ng.2742 – volume: 43 start-page: 977 year: 2011 end-page: 983 ident: CR3 article-title: Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4 publication-title: Nat Genet doi: 10.1038/ng.943 – volume: 150 start-page: 57 year: 2013 end-page: 62 ident: CR26 article-title: Risk of developing diabetes mellitus and hyperlipidemia among patients with bipolar disorder, major depressive disorder, and schizophrenia: a 10-year nationwide population-based prospective cohort study publication-title: J Affect Disord doi: 10.1016/j.jad.2013.02.019 – ident: CR33 – volume: 10 start-page: 168 year: 2014 end-page: 181 ident: CR30 article-title: Mitotic checkpoint proteins Mad1 and Mad2—structural and functional relationship with implication in genetic diseases publication-title: Curr Comput Aided Drug Des doi: 10.2174/1573409910666140410124315 – volume: 47 start-page: 291 year: 2015 end-page: 295 ident: CR18 article-title: LD Score regression distinguishes confounding from polygenicity in genome-wide association studies publication-title: Nat Genet doi: 10.1038/ng.3211 – volume: 467 start-page: 1061 year: 2010 end-page: 1073 ident: CR14 article-title: A map of human genome variation from population-scale sequencing publication-title: Nature doi: 10.1038/nature09534 – volume: 88 start-page: 372 year: 2011 end-page: 381 ident: CR4 article-title: Genome-wide association study identifies genetic variation in neurocan as a susceptibility factor for bipolar disorder publication-title: Am J Hum Genet doi: 10.1016/j.ajhg.2011.01.017 – volume: 5 start-page: 3339 year: 2014 ident: CR7 article-title: Genome-wide association study reveals two new risk loci for bipolar disorder publication-title: Nat Commun doi: 10.1038/ncomms4339 – volume: 29 start-page: 51 year: 2014 end-page: 56 ident: CR28 article-title: Assessment of insulin resistance and metabolic syndrome in drug naive patients of bipolar disorder publication-title: Indian J Clin Biochem doi: 10.1007/s12291-012-0292-x – volume: 150B start-page: 1110 year: 2009 end-page: 1117 ident: CR12 article-title: Preliminary genome-wide association study of bipolar disorder in the Japanese population publication-title: Am J Med Genet doi: 10.1002/ajmg.b.30941 – volume: 26 start-page: 2336 year: 2010 end-page: 2337 ident: CR15 article-title: LocusZoom: regional visualization of genome-wide association scan results publication-title: Bioinformatics doi: 10.1093/bioinformatics/btq419 – volume: 249 start-page: 31 year: 2000 end-page: 45 ident: CR29 article-title: Roles of the NFI/CTF gene family in transcription and development publication-title: Gene doi: 10.1016/S0378-1119(00)00140-2 – volume: 18 start-page: 195 year: 2013 end-page: 205 ident: CR5 article-title: Genome-wide association study meta-analysis of European and Asian-ancestry samples identifies three novel loci associated with bipolar disorder publication-title: Mol Psychiatry doi: 10.1038/mp.2011.157 – volume: 460 start-page: 748 year: 2009 end-page: 752 ident: CR10 article-title: Common polygenic variation contributes to risk of schizophrenia and bipolar disorder publication-title: Nature doi: 10.1038/nature08185 – volume: 10 start-page: 53 year: 2015 ident: CR23 article-title: A genome-wide association study of n-3 and n-6 plasma fatty acids in a Singaporean Chinese population publication-title: Genes Nutr doi: 10.1007/s12263-015-0502-2 – volume: 37 start-page: 294 year: 2015 end-page: 298 ident: CR24 article-title: Increased risk of hyperlipidemia in patients with bipolar disorder: a population-based study publication-title: Gen Hosp Psychiatry doi: 10.1016/j.genhosppsych.2015.04.003 – volume: 45 start-page: 1274 year: 2013 end-page: 1283 ident: CR20 article-title: Discovery and refinement of loci associated with lipid levels publication-title: Nat Genet doi: 10.1038/ng.2797 – volume: 45 start-page: 984 year: 2013 end-page: 994 ident: CR11 article-title: Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs publication-title: Nat Genet doi: 10.1038/ng.2711 – volume: 31 start-page: 1466 year: 2015 end-page: 1468 ident: CR16 article-title: PRSice: Polygenic Risk Score software publication-title: Bioinformatics doi: 10.1093/bioinformatics/btu848 – volume: 381 start-page: 1654 year: 2013 end-page: 1662 ident: CR2 article-title: Genetics of bipolar disorder publication-title: Lancet doi: 10.1016/S0140-6736(13)60855-7 – volume: 19 start-page: 1017 year: 2014 end-page: 1024 ident: CR31 article-title: Polygenic dissection of diagnosis and clinical dimensions of bipolar disorder and schizophrenia publication-title: Mol Psychiatry doi: 10.1038/mp.2013.138 – volume: 99 start-page: 76 year: 2016 end-page: 88 ident: CR19 article-title: Transethnic Genetic-Correlation Estimates from Summary Statistics publication-title: Am J Hum Genet doi: 10.1016/j.ajhg.2016.05.001 – volume: 7 start-page: e1002193 year: 2011 ident: CR22 article-title: Genetic loci associated with plasma phospholipid n-3 fatty acids: a meta-analysis of genome-wide association studies from the CHARGE Consortium publication-title: PLoS Genet doi: 10.1371/journal.pgen.1002193 – volume: 7 start-page: 321 year: 2014 end-page: 331 ident: CR21 article-title: Genome-wide association study of plasma N6 polyunsaturated fatty acids within the cohorts for heart and aging research in genomic epidemiology consortium publication-title: Circ Cardiovasc Genet doi: 10.1161/CIRCGENETICS.113.000208 – volume: 18 start-page: 1302 year: 2013 end-page: 1307 ident: CR6 article-title: Replication of bipolar disorder susceptibility alleles and identification of two novel genome-wide significant associations in a new bipolar disorder case-control sample publication-title: Mol Psychiatry doi: 10.1038/mp.2012.142 – volume: 16 start-page: 548 year: 2011 end-page: 556 ident: CR13 article-title: Genome-wide association study of bipolar I disorder in the Han Chinese population publication-title: Mol Psychiatry doi: 10.1038/mp.2010.43 – volume: 47 start-page: 1228 year: 2015 end-page: 1235 ident: CR17 article-title: Partitioning heritability by functional annotation using genome-wide association summary statistics publication-title: Nat Genet doi: 10.1038/ng.3404 – volume: 126 start-page: 366 year: 2010 end-page: 387 ident: CR25 article-title: Bipolar disorder and metabolic syndrome: an international perspective publication-title: J Affect Disord doi: 10.1016/j.jad.2010.04.012 – volume: 165 start-page: 103 year: 2015 end-page: 107 ident: CR27 article-title: Increased cardiometabolic dysfunction in first-degree relatives of patients with psychotic disorders publication-title: Schizophr Res doi: 10.1016/j.schres.2015.03.034 – volume: 69 start-page: 472 year: 2011 end-page: 478 ident: CR32 article-title: Genome-wide association study of schizophrenia in a Japanese population publication-title: Biol Psychiatry. doi: 10.1016/j.biopsych.2010.07.010 – volume: 99 start-page: 76 year: 2016 ident: BFmp2016259_CR19 publication-title: Am J Hum Genet doi: 10.1016/j.ajhg.2016.05.001 – volume: 150 start-page: 57 year: 2013 ident: BFmp2016259_CR26 publication-title: J Affect Disord doi: 10.1016/j.jad.2013.02.019 – volume: 249 start-page: 31 year: 2000 ident: BFmp2016259_CR29 publication-title: Gene doi: 10.1016/S0378-1119(00)00140-2 – volume: 69 start-page: 472 year: 2011 ident: BFmp2016259_CR32 publication-title: Biol Psychiatry. doi: 10.1016/j.biopsych.2010.07.010 – volume: 10 start-page: 168 year: 2014 ident: BFmp2016259_CR30 publication-title: Curr Comput Aided Drug Des doi: 10.2174/1573409910666140410124315 – volume: 126 start-page: 366 year: 2010 ident: BFmp2016259_CR25 publication-title: J Affect Disord doi: 10.1016/j.jad.2010.04.012 – volume: 19 start-page: 1017 year: 2014 ident: BFmp2016259_CR31 publication-title: Mol Psychiatry doi: 10.1038/mp.2013.138 – volume: 7 start-page: e1002193 year: 2011 ident: BFmp2016259_CR22 publication-title: PLoS Genet doi: 10.1371/journal.pgen.1002193 – volume: 45 start-page: 984 year: 2013 ident: BFmp2016259_CR11 publication-title: Nat Genet doi: 10.1038/ng.2711 – volume: 467 start-page: 1061 year: 2010 ident: BFmp2016259_CR14 publication-title: Nature doi: 10.1038/nature09534 – volume: 26 start-page: 2336 year: 2010 ident: BFmp2016259_CR15 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btq419 – volume: 7 start-page: 321 year: 2014 ident: BFmp2016259_CR21 publication-title: Circ Cardiovasc Genet doi: 10.1161/CIRCGENETICS.113.000208 – volume: 18 start-page: 195 year: 2013 ident: BFmp2016259_CR5 publication-title: Mol Psychiatry doi: 10.1038/mp.2011.157 – volume: 16 start-page: 548 year: 2011 ident: BFmp2016259_CR13 publication-title: Mol Psychiatry doi: 10.1038/mp.2010.43 – volume: 43 start-page: 977 year: 2011 ident: BFmp2016259_CR3 publication-title: Nat Genet doi: 10.1038/ng.943 – volume: 5 start-page: 3339 year: 2014 ident: BFmp2016259_CR7 publication-title: Nat Commun doi: 10.1038/ncomms4339 – volume: 37 start-page: 294 year: 2015 ident: BFmp2016259_CR24 publication-title: Gen Hosp Psychiatry doi: 10.1016/j.genhosppsych.2015.04.003 – volume: 88 start-page: 372 year: 2011 ident: BFmp2016259_CR4 publication-title: Am J Hum Genet doi: 10.1016/j.ajhg.2011.01.017 – volume: 150B start-page: 1110 year: 2009 ident: BFmp2016259_CR12 publication-title: Am J Med Genet doi: 10.1002/ajmg.b.30941 – volume: 165 start-page: 103 year: 2015 ident: BFmp2016259_CR27 publication-title: Schizophr Res doi: 10.1016/j.schres.2015.03.034 – volume: 29 start-page: 51 year: 2014 ident: BFmp2016259_CR28 publication-title: Indian J Clin Biochem doi: 10.1007/s12291-012-0292-x – volume: 381 start-page: 1654 year: 2013 ident: BFmp2016259_CR2 publication-title: Lancet doi: 10.1016/S0140-6736(13)60855-7 – volume: 45 start-page: 1150 year: 2013 ident: BFmp2016259_CR9 publication-title: Nat Genet doi: 10.1038/ng.2742 – volume: 47 start-page: 291 year: 2015 ident: BFmp2016259_CR18 publication-title: Nat Genet doi: 10.1038/ng.3211 – volume: 511 start-page: 421 year: 2014 ident: BFmp2016259_CR8 publication-title: Nature doi: 10.1038/nature13595 – volume: 460 start-page: 748 year: 2009 ident: BFmp2016259_CR10 publication-title: Nature doi: 10.1038/nature08185 – volume: 10 start-page: 53 year: 2015 ident: BFmp2016259_CR23 publication-title: Genes Nutr doi: 10.1007/s12263-015-0502-2 – volume: 25 start-page: 99 year: 2009 ident: BFmp2016259_CR1 publication-title: Trend Genet doi: 10.1016/j.tig.2008.12.002 – volume: 31 start-page: 1466 year: 2015 ident: BFmp2016259_CR16 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btu848 – volume: 47 start-page: 1228 year: 2015 ident: BFmp2016259_CR17 publication-title: Nat Genet doi: 10.1038/ng.3404 – volume: 18 start-page: 1302 year: 2013 ident: BFmp2016259_CR6 publication-title: Mol Psychiatry doi: 10.1038/mp.2012.142 – volume: 45 start-page: 1274 year: 2013 ident: BFmp2016259_CR20 publication-title: Nat Genet doi: 10.1038/ng.2797 – ident: BFmp2016259_CR33 |
SSID | ssj0014765 |
Score | 2.5798836 |
Snippet | Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can... |
SourceID | pubmedcentral proquest gale pubmed crossref springer |
SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
StartPage | 639 |
SubjectTerms | 45/43 631/208 692/699/476/1333 Adult Behavioral Sciences Biological Psychology Bipolar disorder Bipolar Disorder - genetics Cell Cycle Proteins - genetics Chromosome 11 Cytokines - genetics Delta-5 Fatty Acid Desaturase Fatty Acid Desaturases - genetics Female Genetic aspects Genetic Predisposition to Disease - genetics Genome-wide association studies Genome-Wide Association Study Genomes Humans Identification and classification Japan - epidemiology Male Medicine Medicine & Public Health Membrane Glycoproteins - genetics Methods Middle Aged Multifactorial Inheritance - genetics Neurosciences NFI Transcription Factors - genetics Nuclear Proteins - genetics Original original-article Pharmacotherapy Polymorphism, Single Nucleotide - genetics Population Psychiatry Quantitative trait loci Risk factors Susceptibility Systematic review |
SummonAdditionalLinks | – databaseName: Health & Medical Collection dbid: 7X7 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1La9wwEBZtSqGX0vQV51FUSCkU3Pghy9pTWUpDKLSnBvYmbD2oYdd2a2_D_ob86czIsje7hN4MGguhGWlGmk_fEHIeJ3k-U_ksjLTJQgb7ZFhybUKe2hk4VAhQLL4d_vGTX12z74ts4S_cOg-rHPdEt1HrRuEd-QVqM2Jw5OZf2j8hVo3C7KovofGYPEHqMoR05YvpwBWz3JWSjNMMs52C-fd5USouVshVGfPPCZKU3vNI-_vyPce0D5rcy5w6h3T5gjz3kSSdD6o_JI9M_ZI8HWpLbl6R2zlF_tWVCW8qbWixVQN1lLK00gNQyHS0v2lo3fwzS9qtO4dzcZDZDQVPV9Gi1rRHl0bbqdoXfC430H-lUGzs3GiK97q0rFo8MVPtqT1fk-vLb7--XoW-8kKoIBzqQxtFikUWnL3libAws5HltkhTa1WkijwtDRelLU2mCisEi5lOiplmjCnLGQi-IQd1U5sjQgvFC2XSMmXCMKEgQNA60RpDSxVZUwbk0zj7UnlacqyOsZQuPZ4KuWolqkqCqgJyPgm3AxvHw2IfUY0S1yj0pQr_1ABGhGxXcp4hBxZEUnlATnckYW2p3ebREKRf253cWmJA3k_N-Cfi1WrTrDsZCx5zd9gOyNvBbqYBQ-dxlmNLvmNRkwAyfu-21NVvx_ydIeaXiYB8GG1vO6wH5uH4_8M_Ic9AUgyIulNy0P9dmzMIsfrynVtHd7QjKUg priority: 102 providerName: ProQuest |
Title | A genome-wide association study identifies two novel susceptibility loci and trans population polygenicity associated with bipolar disorder |
URI | https://link.springer.com/article/10.1038/mp.2016.259 https://www.ncbi.nlm.nih.gov/pubmed/28115744 https://www.proquest.com/docview/2004041946 https://www.proquest.com/docview/1861606144 https://pubmed.ncbi.nlm.nih.gov/PMC5822448 |
Volume | 23 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3da9swED_Wlo29jK378tYFDToGA292LMvyYxIayqBhjBXyZmx9UEPihNlZyd-wf3p3_mod-rAnC3SWhXTSnXw__Q7g3B9HUayi2PW0CV2O-6SbCW1cEdgYDSo6KJbuDl8txOU1_74Mly3PdtnCKhtKy3qb7tBh39bELemLr-itH8EJcbaTOs_ErA8Z8KjOG-kHIYU2JW8v43mBvP_ywPwcbsL3rNAhQvIgTFpbn_lzeNa6jWzSdPQFPDLFKTxuEknuT-HJVRsifwl_J4x4V9fGvc21Yend8LOaSpblugEImZJVtxtWbP6YFSt3ZY1vqaGye4YWLmdpoVlFpoxt-yxfWFztsX38GIp1jRvN6H8uy_ItnZSZbik9X8H1_OLX7NJtMy64Ct2gyrWep7hn0chbMZY2DqVnhU2DwFrlqTQKMiNkZjMTqtRKyX2ux2msOefKCo6Cr-G42BTmLbBUiVSZIAu4NFwqdAy0HmtNLqXyrMkc-NJNRKJaOnLKirFK6rB4IJP1NqFZS3DWHDjvhbcNC8fDYp9pRhNam9iWStsrBtgjYrlKJiFxX6EHFTlwNpDENaWG1Z1OJO2aLilhJ_e4H3PhwMe-mt4knFphNrsy8aXwRX3IduBNo0J9h7FxP4yoJhooVy9ATN_DmiK_qRm_Q8L6cunAp04N77r1wDi8-0-59_AUi7KB1J3BcfV7Zz6gj1VlIziKltEITibz6XSBz-nF4sfPUb3i_gHc5yvE |
linkProvider | Springer Nature |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Zb9NAEF6VVAheEDeGAovUCgnJ1Md6vX5AKECrlLYRQq3Ut629h7CUOAEnRPkN_Bd-IzO-0kQVb32ztOPRyjM7h2f2G0J2_SCOExUnrqdN5DKwk27GtXF5aBNwqBCgWLw7fDrkg3P29SK62CJ_27sw2FbZ2sTKUOuJwn_k-yhNj0HKzT9Of7o4NQqrq-0IjVotjs1yASlb-eHoC8h3LwgOD84-D9xmqoCrwNXPXOt5inkWHJnlgbBJJDzLbRqG1ipPpXGYGS4ym5lIpVYI5jMdpIlmjCnLGRAC31tkm4WQyvTI9qeD4bfvXd2CxdXwSj-MsL4qWHMj0AvF_hjRMX3-PkBY1Cs-cNMTXHGFm22aG7XaygUe3if3mtiV9mtle0C2TPGQ3K6nWS4fkT99ioivY-Mucm1ouhI8rUBsaa7r1iRT0tliQovJbzOi5bysOmuqJt0lBd-a07TQdIZOlE67-WLwOFoC_1whWcvcaIp_kmmWTzFHp7oBE31Mzm9EKk9Ir5gU5hmhqeKpMmEWMmGYUBCSaB1ojcGs8qzJHPKu_fpSNUDoOI9jJKuCfCjkeCpRVBJE5ZDdjnha439cT_YWxSjRKgAvlTaXG2BHiK8l-xGibkHsFjtkZ40STrNaX24VQTbWpJQr3XfIm24Z38QOucJM5qX0Bfd5ld475GmtN92GgbkfxbgSr2lUR4AY4-srRf6jwhqPsMuYCYfstbq32tY13-H5_7f_mtwZnJ2eyJOj4fELchfeEnU_3w7pzX7NzUsI8GbZq-ZUUXJ50wf5H4BnaTc |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1ba9RAFB5qRfFFvButOkKLIKSby2QyeRBZrEtrtfhgYd_GZC4Y2M1um6zL_gb_kb_Oc3Lb7lJ861tgTg5Dzj1z5juE7PtBHCcqTlxPm8hl4CfdjGvj8tAmEFAhQbF4d_jbGT8-Z1_G0XiH_O3uwmBbZecTa0etZwr_kQ9Qmh6DkpsPbNsW8f1o9HF-4eIEKTxp7cZpNCpyalZLKN_KDydHIOuDIBh9_vHp2G0nDLgKwn7lWs9TzLMQ1CwPhE0i4Vlu0zC0VnkqjcPMcJHZzEQqtUIwn-kgTTRjTFnOgBD43iK34zDy0cbicV_s-Syux1j6YYQnrYK1dwO9UAymiJPp88MAAVKvRMPtmHAlKG43bG6d2tbBcPSA3G-zWDps1O4h2THFI3KnmWu5ekz-DCliv06Nu8y1oelaBWgNZ0tz3TQpmZJWyxktZr_NhJaLsu6xqdt1VxSibE7TQtMKwymd95PG4HGyAv65QrKOudEU_ynTLJ9jtU51Cyv6hJzfiEyekt1iVpjnhKaKp8qEWciEYUJBcqJ1oDWmtcqzJnPI--7rS9VCouNkjomsj-ZDIadziaKSICqH7PfE8wYJ5HqydyhGif4BeKm0veYAO0KkLTmMEH8LsrjYIXsblGDXanO5UwTZ-pVSrq3AIW_7ZXwTe-UKM1uU0hfc53Wh75Bnjd70GwbmfhTjSryhUT0Boo1vrhT5rxp1PMJ-YyYcctDp3npb13yHF__f_htyF8xXfj05O31J7sFLomns2yO71eXCvIJMr8pe1yZFyc-btuF_9ZtsBw |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=A+genome-wide+association+study+identifies+two+novel+susceptibility+loci+and+trans+population+polygenicity+associated+with+bipolar+disorder&rft.jtitle=Molecular+psychiatry&rft.au=Ikeda%2C+M&rft.au=Takahashi%2C+A&rft.au=Kamatani%2C+Y&rft.au=Okahisa%2C+Y&rft.date=2018-03-01&rft.pub=Nature+Publishing+Group+UK&rft.issn=1359-4184&rft.eissn=1476-5578&rft.volume=23&rft.issue=3&rft.spage=639&rft.epage=647&rft_id=info:doi/10.1038%2Fmp.2016.259&rft.externalDocID=10_1038_mp_2016_259 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1359-4184&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1359-4184&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1359-4184&client=summon |