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...

Full description

Saved in:
Bibliographic Details
Published inMolecular psychiatry Vol. 23; no. 3; pp. 639 - 647
Main Authors Ikeda, M, Takahashi, A, Kamatani, Y, Okahisa, Y, Kunugi, H, Mori, N, Sasaki, T, Ohmori, T, Okamoto, Y, Kawasaki, H, Shimodera, S, Kato, T, Yoneda, H, Yoshimura, R, Iyo, M, Matsuda, K, Akiyama, M, Ashikawa, K, Kashiwase, K, Tokunaga, K, Kondo, K, Saito, T, Shimasaki, A, Kawase, K, Kitajima, T, Matsuo, K, Itokawa, M, Someya, T, Inada, T, Hashimoto, R, Inoue, T, Akiyama, K, Tanii, H, Arai, H, Kanba, S, Ozaki, N, Kusumi, I, Yoshikawa, T, Kubo, M, Iwata, N
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.03.2018
Nature Publishing Group
Subjects
Online AccessGet 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