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Article: Common variants conferring risk of schizophrenia
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TitleCommon variants conferring risk of schizophrenia
 
AuthorsStefansson, H
Ophoff, RA39 16
Steinberg, S
Andreassen, OA30
Cichon, S4
Rujescu, D
Werge, T1
Pietiläinen, OPH29 22
Mors, O35
Mortensen, PB10
Sigurdsson, E8 21
Gustafsson, O
Nyegaard, M10
TuulioHenriksson, A23
Ingason, A
Hansen, T1
Suvisaari, J23
Lonnqvist, J23
Paunio, T23
Børglum, AD35 10
Hartmann, A
FinkJensen, A28
Nordentoft, M20
Hougaard, D14
NorgaardPedersen, B14
Böttcher, Y
Olesen, J17
Breuer, R18
Möller, HJ2
Giegling, I
Rasmussen, HB1
Timm, S1
Mattheisen, M4
Bitter, I37
Réthelyi, JM37
Magnusdottir, BB8 21
Sigmundsson, T8 21
Olason, P
Masson, G
Gulcher, JR
Haraldsson, M8 21
Fossdal, R
Thorgeirsson, TE
Thorsteinsdottir, U21
Ruggeri, M36
Tosato, S36
Franke, B31
Strengman, E39
Kiemeney, LA31
Melle, I30
Djurovic, S30
Abramova, L19
Kaleda, V19
Sanjuan, J13
De Frutos, R25
Bramon, E3
Vassos, E3
Fraser, G5
Ettinger, U3
Picchioni, M3
Walker, N24
Toulopoulou, T3
Need, AC34
Ge, D34
Lim Yoon, J33
Shianna, KV34
Freimer, NB16
Cantor, RM16 33
Murray, R3
Kong, A
Golimbet, V19
Carracedo, A11
Arango, C9
Costas, J32
Jönsson, EG27
Terenius, L27
Agartz, I27
Petursson, H8 21
Nöthen, MM4
Rietschel, M18
Matthews, PM6
Muglia, P15
Peltonen, L29 22
St Clair, D5
Goldstein, DB34
Stefansson, K21
Collier, DA3 38
Kahn, RS39
Linszen, DH7
Van Os, J26
Wiersma, D12
Bruggeman, R12
Cahn, W39
De Haan, L7
Krabbendam, L26
MyinGermeys, I26
 
KeywordsChemicals And Cas Registry Numbers
 
Issue Date2009
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nature
 
CitationNature, 2009, v. 460 n. 7256, p. 744-747 [How to Cite?]
DOI: http://dx.doi.org/10.1038/nature08186
 
AbstractSchizophrenia is a complex disorder, caused by both genetic and environmental factors and their interactions. Research on pathogenesis has traditionally focused on neurotransmitter systems in the brain, particularly those involving dopamine. Schizophrenia has been considered a separate disease for over a century, but in the absence of clear biological markers, diagnosis has historically been based on signs and symptoms. A fundamental message emerging from genome-wide association studies of copy number variations (CNVs) associated with the disease is that its genetic basis does not necessarily conform to classical nosological disease boundaries. Certain CNVs confer not only high relative risk of schizophrenia but also of other psychiatric disorders. The structural variations associated with schizophrenia can involve several genes and the phenotypic syndromes, or the ĝ€ genomic disordersĝ€™, have not yet been characterized. Single nucleotide polymorphism (SNP)-based genome-wide association studies with the potential to implicate individual genes in complex diseases may reveal underlying biological pathways. Here we combined SNP data from several large genome-wide scans and followed up the most significant association signals. We found significant association with several markers spanning the major histocompatibility complex (MHC) region on chromosome 6p21.3-22.1, a marker located upstream of the neurogranin gene (NRGN) on 11q24.2 and a marker in intron four of transcription factor 4 (TCF4) on 18q21.2. Our findings implicating the MHC region are consistent with an immune component to schizophrenia risk, whereas the association with NRGN and TCF4 points to perturbation of pathways involved in brain development, memory and cognition. © 2009 Macmillan Publishers Limited.
 
ISSN0028-0836
2013 Impact Factor: 42.351
 
DOIhttp://dx.doi.org/10.1038/nature08186
 
PubMed Central IDPMC3077530
PMC3077530
 
ISI Accession Number IDWOS:000268670300040
Funding AgencyGrant Number
EULSHM-CT-2006-037761
PIAP-GA-2008-218251
HEALTH-F2-2009-223423
NIMHR01 MH078075
German Federal Ministry of Education and ResearchNGFN-2
Marie CuriePIAP-GA-2008-218251
GlaxoSmithKline
National Institutes of Health1R01HL087679-01
STAMPEED
Funding Information:

We thank the subjects and their relatives and staff at the recruitment centres. This work was sponsored by EU grants LSHM-CT-2006-037761 (Project SGENE), PIAP-GA-2008-218251 (Project PsychGene) and HEALTH-F2-2009-223423 (Project PsychCNVs). Genotyping of the Dutch samples was sponsored by NIMH funding, R01 MH078075. This work was also supported by the National Genomic Network (NGFN-2) of the German Federal Ministry of Education and Research (BMBF) and Marie Curie grant PIAP-GA-2008-218251 (PsychGene). M. M. N. received support from the Alfried Krupp von Bohlen und Halbach-Stiftung. We are grateful to S. Schreiber and M. Krawczak for providing genotype data for PopGen controls, and to K.-H. Jockel and R. Erbel for providing control individuals from the Heinz Nixdorf Recall Study. Recruitment of the patients from Munich was partially supported by GlaxoSmithKline. We are grateful to the Genetics Research Centre GmbH, an initiative by GlaxoSmithKline and LMU. The Northern Finland Birth Cohort 1966 (NFBC66) is thanked for providing population controls for the study. The genotyping of NFBC66 was financially supported by National Institutes of Health grant 1R01HL087679-01, STAMPEED.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorStefansson, H
 
dc.contributor.authorOphoff, RA
 
dc.contributor.authorSteinberg, S
 
dc.contributor.authorAndreassen, OA
 
dc.contributor.authorCichon, S
 
dc.contributor.authorRujescu, D
 
dc.contributor.authorWerge, T
 
dc.contributor.authorPietiläinen, OPH
 
dc.contributor.authorMors, O
 
dc.contributor.authorMortensen, PB
 
dc.contributor.authorSigurdsson, E
 
dc.contributor.authorGustafsson, O
 
dc.contributor.authorNyegaard, M
 
dc.contributor.authorTuulioHenriksson, A
 
dc.contributor.authorIngason, A
 
dc.contributor.authorHansen, T
 
dc.contributor.authorSuvisaari, J
 
dc.contributor.authorLonnqvist, J
 
dc.contributor.authorPaunio, T
 
dc.contributor.authorBørglum, AD
 
dc.contributor.authorHartmann, A
 
dc.contributor.authorFinkJensen, A
 
dc.contributor.authorNordentoft, M
 
dc.contributor.authorHougaard, D
 
dc.contributor.authorNorgaardPedersen, B
 
dc.contributor.authorBöttcher, Y
 
dc.contributor.authorOlesen, J
 
dc.contributor.authorBreuer, R
 
dc.contributor.authorMöller, HJ
 
dc.contributor.authorGiegling, I
 
dc.contributor.authorRasmussen, HB
 
dc.contributor.authorTimm, S
 
dc.contributor.authorMattheisen, M
 
dc.contributor.authorBitter, I
 
dc.contributor.authorRéthelyi, JM
 
dc.contributor.authorMagnusdottir, BB
 
dc.contributor.authorSigmundsson, T
 
dc.contributor.authorOlason, P
 
dc.contributor.authorMasson, G
 
dc.contributor.authorGulcher, JR
 
dc.contributor.authorHaraldsson, M
 
dc.contributor.authorFossdal, R
 
dc.contributor.authorThorgeirsson, TE
 
dc.contributor.authorThorsteinsdottir, U
 
dc.contributor.authorRuggeri, M
 
dc.contributor.authorTosato, S
 
dc.contributor.authorFranke, B
 
dc.contributor.authorStrengman, E
 
dc.contributor.authorKiemeney, LA
 
dc.contributor.authorMelle, I
 
dc.contributor.authorDjurovic, S
 
dc.contributor.authorAbramova, L
 
dc.contributor.authorKaleda, V
 
dc.contributor.authorSanjuan, J
 
dc.contributor.authorDe Frutos, R
 
dc.contributor.authorBramon, E
 
dc.contributor.authorVassos, E
 
dc.contributor.authorFraser, G
 
dc.contributor.authorEttinger, U
 
dc.contributor.authorPicchioni, M
 
dc.contributor.authorWalker, N
 
dc.contributor.authorToulopoulou, T
 
dc.contributor.authorNeed, AC
 
dc.contributor.authorGe, D
 
dc.contributor.authorLim Yoon, J
 
dc.contributor.authorShianna, KV
 
dc.contributor.authorFreimer, NB
 
dc.contributor.authorCantor, RM
 
dc.contributor.authorMurray, R
 
dc.contributor.authorKong, A
 
dc.contributor.authorGolimbet, V
 
dc.contributor.authorCarracedo, A
 
dc.contributor.authorArango, C
 
dc.contributor.authorCostas, J
 
dc.contributor.authorJönsson, EG
 
dc.contributor.authorTerenius, L
 
dc.contributor.authorAgartz, I
 
dc.contributor.authorPetursson, H
 
dc.contributor.authorNöthen, MM
 
dc.contributor.authorRietschel, M
 
dc.contributor.authorMatthews, PM
 
dc.contributor.authorMuglia, P
 
dc.contributor.authorPeltonen, L
 
dc.contributor.authorSt Clair, D
 
dc.contributor.authorGoldstein, DB
 
dc.contributor.authorStefansson, K
 
dc.contributor.authorCollier, DA
 
dc.contributor.authorKahn, RS
 
dc.contributor.authorLinszen, DH
 
dc.contributor.authorVan Os, J
 
dc.contributor.authorWiersma, D
 
dc.contributor.authorBruggeman, R
 
dc.contributor.authorCahn, W
 
dc.contributor.authorDe Haan, L
 
dc.contributor.authorKrabbendam, L
 
dc.contributor.authorMyinGermeys, I
 
dc.date.accessioned2011-09-27T03:02:57Z
 
dc.date.available2011-09-27T03:02:57Z
 
dc.date.issued2009
 
dc.description.abstractSchizophrenia is a complex disorder, caused by both genetic and environmental factors and their interactions. Research on pathogenesis has traditionally focused on neurotransmitter systems in the brain, particularly those involving dopamine. Schizophrenia has been considered a separate disease for over a century, but in the absence of clear biological markers, diagnosis has historically been based on signs and symptoms. A fundamental message emerging from genome-wide association studies of copy number variations (CNVs) associated with the disease is that its genetic basis does not necessarily conform to classical nosological disease boundaries. Certain CNVs confer not only high relative risk of schizophrenia but also of other psychiatric disorders. The structural variations associated with schizophrenia can involve several genes and the phenotypic syndromes, or the ĝ€ genomic disordersĝ€™, have not yet been characterized. Single nucleotide polymorphism (SNP)-based genome-wide association studies with the potential to implicate individual genes in complex diseases may reveal underlying biological pathways. Here we combined SNP data from several large genome-wide scans and followed up the most significant association signals. We found significant association with several markers spanning the major histocompatibility complex (MHC) region on chromosome 6p21.3-22.1, a marker located upstream of the neurogranin gene (NRGN) on 11q24.2 and a marker in intron four of transcription factor 4 (TCF4) on 18q21.2. Our findings implicating the MHC region are consistent with an immune component to schizophrenia risk, whereas the association with NRGN and TCF4 points to perturbation of pathways involved in brain development, memory and cognition. © 2009 Macmillan Publishers Limited.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationNature, 2009, v. 460 n. 7256, p. 744-747 [How to Cite?]
DOI: http://dx.doi.org/10.1038/nature08186
 
dc.identifier.citeulike5103475
 
dc.identifier.doihttp://dx.doi.org/10.1038/nature08186
 
dc.identifier.eissn1476-4687
 
dc.identifier.epage747
 
dc.identifier.f10002136989
 
dc.identifier.f10002136989
 
dc.identifier.f10002136989
 
dc.identifier.isiWOS:000268670300040
Funding AgencyGrant Number
EULSHM-CT-2006-037761
PIAP-GA-2008-218251
HEALTH-F2-2009-223423
NIMHR01 MH078075
German Federal Ministry of Education and ResearchNGFN-2
Marie CuriePIAP-GA-2008-218251
GlaxoSmithKline
National Institutes of Health1R01HL087679-01
STAMPEED
Funding Information:

We thank the subjects and their relatives and staff at the recruitment centres. This work was sponsored by EU grants LSHM-CT-2006-037761 (Project SGENE), PIAP-GA-2008-218251 (Project PsychGene) and HEALTH-F2-2009-223423 (Project PsychCNVs). Genotyping of the Dutch samples was sponsored by NIMH funding, R01 MH078075. This work was also supported by the National Genomic Network (NGFN-2) of the German Federal Ministry of Education and Research (BMBF) and Marie Curie grant PIAP-GA-2008-218251 (PsychGene). M. M. N. received support from the Alfried Krupp von Bohlen und Halbach-Stiftung. We are grateful to S. Schreiber and M. Krawczak for providing genotype data for PopGen controls, and to K.-H. Jockel and R. Erbel for providing control individuals from the Heinz Nixdorf Recall Study. Recruitment of the patients from Munich was partially supported by GlaxoSmithKline. We are grateful to the Genetics Research Centre GmbH, an initiative by GlaxoSmithKline and LMU. The Northern Finland Birth Cohort 1966 (NFBC66) is thanked for providing population controls for the study. The genotyping of NFBC66 was financially supported by National Institutes of Health grant 1R01HL087679-01, STAMPEED.

 
dc.identifier.issn0028-0836
2013 Impact Factor: 42.351
 
dc.identifier.issue7256
 
dc.identifier.pmcidPMC3077530
 
dc.identifier.pmcidPMC3077530
 
dc.identifier.pmid19571808
 
dc.identifier.scopuseid_2-s2.0-68449090594
 
dc.identifier.spage744
 
dc.identifier.urihttp://hdl.handle.net/10722/141836
 
dc.identifier.volume460
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nature
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofNature
 
dc.relation.referencesReferences in Scopus
 
dc.subjectChemicals And Cas Registry Numbers
 
dc.titleCommon variants conferring risk of schizophrenia
 
dc.typeArticle
 
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Author Affiliations
  1. Copenhagen University Hospital
  2. Ludwig-Maximilians-Universität München
  3. King's College London
  4. Universität Bonn
  5. University of Aberdeen
  6. Hammersmith Hospital
  7. Academic Medical Centre, University of Amsterdam
  8. National University Hospital Reykjavik
  9. Hospital General Universitario Gregorio Marañon
  10. Aarhus Universitet
  11. Universidad de Santiago de Compostela
  12. Universitair Medisch Centrum Groningen
  13. Universitat de Valencia, Facultad de Medicina y Odontologia
  14. Statens Serum Institut
  15. GlaxoSmithKline
  16. UCLA Medical Center
  17. Amtssygehuset i Glostrup
  18. Universität Heidelberg
  19. Russian Academy of Medical Sciences
  20. Bispebjerg Hospital
  21. University of Iceland
  22. Wellcome Trust Sanger Institute
  23. Kansanterveyslaitos
  24. Ravenscraig Hospital
  25. Universitat de Valencia
  26. Maastricht University
  27. Karolinska Institutet
  28. Rigshospitalet
  29. Institute for Molecular Medicine
  30. Universitetet i Oslo
  31. Radboud University Nijmegen Medical Centre
  32. Fundacioarolinan Puarolinablica Galega de Medicina Xenoarolinamica
  33. University of California, Los Angeles
  34. Duke Institute for Genome Sciences &amp; Policy
  35. Ârhus Universitetshospital
  36. Università degli Studi di Verona
  37. Semmelweis Egyetem
  38. Sichuan University
  39. University Medical Center Utrecht