Rare chromosomal deletions and duplications increase risk of schizophrenia
Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73-90% (ref. 1). Inheritance patterns are complex, and the number and type of genetic variants involved are not understood. Copy number variants (CNVs) have...
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Published in | Nature Vol. 455; no. 7210; pp. 237 - 241 |
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Main Authors | , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
11.09.2008
Nature Publishing Nature Publishing Group |
Subjects | |
Online Access | Get full text |
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Abstract | Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73-90% (ref. 1). Inheritance patterns are complex, and the number and type of genetic variants involved are not understood. Copy number variants (CNVs) have been identified in individual patients with schizophrenia and also in neurodevelopmental disorders, but large-scale genome-wide surveys have not been performed. Here we report a genome-wide survey of rare CNVs in 3,391 patients with schizophrenia and 3,181 ancestrally matched controls, using high-density microarrays. For CNVs that were observed in less than 1% of the sample and were more than 100 kilobases in length, the total burden is increased 1.15-fold in patients with schizophrenia in comparison with controls. This effect was more pronounced for rarer, single-occurrence CNVs and for those that involved genes as opposed to those that did not. As expected, deletions were found within the region critical for velo-cardio-facial syndrome, which includes psychotic symptoms in 30% of patients. Associations with schizophrenia were also found for large deletions on chromosome 15q13.3 and 1q21.1. These associations have not previously been reported, and they remained significant after genome-wide correction. Our results provide strong support for a model of schizophrenia pathogenesis that includes the effects of multiple rare structural variants, both genome-wide and at specific loci. |
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AbstractList | Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73-90%. Inheritance patterns are complex, and the number and type of genetic variants involved are not understood. Copy number variants (CNVs) have been identified in individual patients with schizophrenia and also in neurodevelopmental disorders, but large-scale genome-wide surveys have not been performed. Here we report a genome-wide survey of rare CNVs in 3,391 patients with schizophrenia and 3,181 ancestrally matched controls, using high-density microarrays. For CNVs that were observed in less than 1% of the sample and were more than 100 kilobases in length, the total burden is increased 1.15-fold in patients with schizophrenia in comparison with controls. This effect was more pronounced for rarer, single-occurrence CNVs and for those that involved genes as opposed to those that did not. As expected, deletions were found within the region critical for velo-cardio- facial syndrome, which includes psychotic symptoms in 30% of patients. Associations with schizophrenia were also found for large deletions on chromosome 15q13.3 and 1q21.1. These associations have not previously been reported, and they remained significant after genome-wide correction. Our results provide strong support for a model of schizophrenia pathogenesis that includes the effects of multiple rare structural variants, both genome-wide and at specific loci. Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73-90% (ref. 1). Inheritance patterns are complex, and the number and type of genetic variants involved are not understood. Copy number variants (CNVs) have been identified in individual patients with schizophrenia and also in neurodevelopmental disorders, but large-scale genome-wide surveys have not been performed. Here we report a genome-wide survey of rare CNVs in 3,391 patients with schizophrenia and 3,181 ancestrally matched controls, using high-density microarrays. For CNVs that were observed in less than 1% of the sample and were more than 100 kilobases in length, the total burden is increased 1.15-fold in patients with schizophrenia in comparison with controls. This effect was more pronounced for rarer, single-occurrence CNVs and for those that involved genes as opposed to those that did not. As expected, deletions were found within the region critical for velo-cardio-facial syndrome, which includes psychotic symptoms in 30% of patients. Associations with schizophrenia were also found for large deletions on chromosome 15q13.3 and 1q21.1. These associations have not previously been reported, and they remained significant after genome-wide correction. Our results provide strong support for a model of schizophrenia pathogenesis that includes the effects of multiple rare structural variants, both genome-wide and at specific loci. [PUBLICATION ABSTRACT] Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73-90% (ref. 1). Inheritance patterns are complex, and the number and type of genetic variants involved are not understood. Copy number variants (CNVs) have been identified in individual patients with schizophrenia and also in neurodevelopmental disorders, but large-scale genome-wide surveys have not been performed. Here we report a genome-wide survey of rare CNVs in 3,391 patients with schizophrenia and 3,181 ancestrally matched controls, using high-density microarrays. For CNVs that were observed in less than 1% of the sample and were more than 100 kilobases in length, the total burden is increased 1.15-fold in patients with schizophrenia in comparison with controls. This effect was more pronounced for rarer, single-occurrence CNVs and for those that involved genes as opposed to those that did not. As expected, deletions were found within the region critical for velo-cardio-facial syndrome, which includes psychotic symptoms in 30% of patients. Associations with schizophrenia were also found for large deletions on chromosome 15q13.3 and 1q21.1. These associations have not previously been reported, and they remained significant after genome-wide correction. Our results provide strong support for a model of schizophrenia pathogenesis that includes the effects of multiple rare structural variants, both genome-wide and at specific loci. The genetics of schizophrenia The genetics of schizophrenia and other mental disorders are complex and poorly understood, and made even harder to study because reduced reproduction rates result in negative selection pressure on risk alleles. To date, some copy number variations have been linked to schizophrenia but the studies have been relatively small. Now two independent large-scale genome-wide studies of thousands of patients and controls by two international consortia confirm a previously identified locus but also reveal novel associations. In the first study, a collaboration between SGENE and partners, de novo (spontaneous) copy number variants are reported on chromosomes 1 and 15. In the second study, by the International Schizophrenia Consortium, deletions were also reported on these chromosomes, as was greater overall frequency of copy number variation in the genome. The genetics of schizophrenia and other mental disorders are complex and poorly understood, and made even harder to study due to reduced reproduction resulting in negative selection pressure on risk alleles. Two independent large-scale genome wide studies of thousands of patients and controls by two international consortia confirm a previously identified locus, but also reveal novel associations. In this study, deletions were reported on chromosomes 1 and 15, as well as a greater overall frequency of copy number variation in the genome. Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73–90% (ref. 1 ). Inheritance patterns are complex, and the number and type of genetic variants involved are not understood. Copy number variants (CNVs) have been identified in individual patients with schizophrenia 2 , 3 , 4 , 5 , 6 , 7 and also in neurodevelopmental disorders 8 , 9 , 10 , 11 , but large-scale genome-wide surveys have not been performed. Here we report a genome-wide survey of rare CNVs in 3,391 patients with schizophrenia and 3,181 ancestrally matched controls, using high-density microarrays. For CNVs that were observed in less than 1% of the sample and were more than 100 kilobases in length, the total burden is increased 1.15-fold in patients with schizophrenia in comparison with controls. This effect was more pronounced for rarer, single-occurrence CNVs and for those that involved genes as opposed to those that did not. As expected, deletions were found within the region critical for velo-cardio-facial syndrome, which includes psychotic symptoms in 30% of patients 12 . Associations with schizophrenia were also found for large deletions on chromosome 15q13.3 and 1q21.1. These associations have not previously been reported, and they remained significant after genome-wide correction. Our results provide strong support for a model of schizophrenia pathogenesis that includes the effects of multiple rare structural variants, both genome-wide and at specific loci. Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73 - 90% ( ref. 1). Inheritance patterns are complex, and the number and type of genetic variants involved are not understood. Copy number variants ( CNVs) have been identified in individual patients with schizophrenia(2-7) and also in neurodevelopmental disorders(8-11), but large- scale genome- wide surveys have not been performed. Here we report a genome- wide survey of rare CNVs in 3,391 patients with schizophrenia and 3,181 ancestrally matched controls, using high- density microarrays. For CNVs that were observed in less than 1% of the sample and were more than 100 kilobases in length, the total burden is increased 1.15- fold in patients with schizophrenia in comparison with controls. This effect was more pronounced for rarer, single- occurrence CNVs and for those that involved genes as opposed to those that did not. As expected, deletions were found within the region critical for velo- cardio- facial syndrome, which includes psychotic symptoms in 30% of patients(12). Associations with schizophrenia were also found for large deletions on chromosome 15q13.3 and 1q21.1. These associations have not previously been reported, and they remained significant after genome- wide correction. Our results provide strong support for a model of schizophrenia pathogenesis that includes the effects of multiple rare structural variants, both genome- wide and at specific loci. |
Audience | Academic |
Author | Stone, Jennifer L. Craddock, Nick J. Kirov, George K. Purcell, Shaun M. O'Donovan, Michael C. McQuillin, Andrew Blackwood, Douglas H. R. Sullivan, Patrick F. Gill, Michael Corvin, Aiden Gurling, Hugh Ruderfer, Douglas M. Owen, Michael J. Sklar, Pamela St Clair, David Lichtenstein, Paul Hultman, Christina M. Pato, Carlos N. |
Author_xml | – sequence: 1 givenname: Jennifer L. surname: Stone fullname: Stone, Jennifer L. – sequence: 2 givenname: Michael C. surname: O'Donovan fullname: O'Donovan, Michael C. – sequence: 3 givenname: Hugh surname: Gurling fullname: Gurling, Hugh – sequence: 4 givenname: George K. surname: Kirov fullname: Kirov, George K. – sequence: 5 givenname: Douglas H. R. surname: Blackwood fullname: Blackwood, Douglas H. R. – sequence: 6 givenname: Aiden surname: Corvin fullname: Corvin, Aiden – sequence: 7 givenname: Nick J. surname: Craddock fullname: Craddock, Nick J. – sequence: 8 givenname: Michael surname: Gill fullname: Gill, Michael – sequence: 9 givenname: Christina M. surname: Hultman fullname: Hultman, Christina M. organization: Psykiatri, Akademiska sjukhuset – sequence: 10 givenname: Paul surname: Lichtenstein fullname: Lichtenstein, Paul – sequence: 11 givenname: Andrew surname: McQuillin fullname: McQuillin, Andrew – sequence: 12 givenname: Carlos N. surname: Pato fullname: Pato, Carlos N. – sequence: 13 givenname: Douglas M. surname: Ruderfer fullname: Ruderfer, Douglas M. – sequence: 14 givenname: Michael J. surname: Owen fullname: Owen, Michael J. – sequence: 15 givenname: David surname: St Clair fullname: St Clair, David – sequence: 16 givenname: Patrick F. surname: Sullivan fullname: Sullivan, Patrick F. – sequence: 17 givenname: Pamela surname: Sklar fullname: Sklar, Pamela – sequence: 18 givenname: Shaun M. surname: Purcell fullname: Purcell, Shaun M. |
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ContentType | Journal Article |
Contributor | Holmans, Peter A Fraser, Gillian Thelander, Emma F Pickard, Ben Puri, Vinay Krasucki, Robert Walker, Nicholas Gurling, Hugh St Clair, David Datta, Susmita O'Donovan, Michael C Pato, Michele T Visscher, Peter M Ruderfer, Douglas M Choudhury, Khalid Toncheva, Draga Pato, Carlos N Sullivan, Patrick F Daly, Mark J Van Beck, Margaret Craddock, Nick J Blackwood, Douglas H R Muir, Walter J Hultman, Christina M Sklar, Pamela Lichtenstein, Paul Kwan, Soh Leh Purcell, Shaun M Stone, Jennifer L Lawrence, Jacob Scolnick, Edward M McGhee, Kevin A McQuillin, Andrew Macgregor, Stuart Pimm, Jonathan Curtis, David O'Dushlaine, Colm T Milanova, Vihra Kirov, George K Maclean, Alan W Norton, N Korn, Joshua Owen, Michael J Morris, Derek W Kenny, Elaine Waddington, John L Georgieva, Lucy Williams, Nigel M Nikolov, Ivan Gill, Michael Thirumalai, Srinivasa Bass, Nicholas Corvin, Aiden Malloy, Pat Williams, H Sullivan, Patrick Quested, Digby Crombie, Caroline |
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Copyright | Macmillan Publishers Limited. All rights reserved 2008 2008 INIST-CNRS COPYRIGHT 2008 Nature Publishing Group Copyright Nature Publishing Group Sep 11, 2008 |
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References | Kirov, G. (b3) 2008; 17 Shaikh, T. H. (b28) 2007; 17 (b31) 2000 Korn, J. (b15) Moon, H. J. (b7) 2006; 344 Sullivan, P. F., Kendler, K. S., Neale, M. C. (b1) 2003; 60 Weiss, L. A. (b10) 2008; 358 Stankiewicz, P., Lupski, J. R. (b27) 2002; 18 Lee, J. A., Lupski, J. R. (b11) 2006; 52 Flomen, R. H. (b4) 2006; 141 Sebat, J. (b9) 2007; 316 Sharp, A. J. (b24) 2006; 38 Lee, J. A., Carvalho, C. M., Lupski, J. R. A. (b29) 2007; 131 Friedman, J. I. (b5) 2008; 13 Butler, M. G., Fischer, W., Kibiryeva, N., Bittel, D. C. (b21) 2008; 146 Stefansson, H. ( 10.1038/nature07229 b30) Xu, J. (b23) 2001; 105 Gurling, H. M. (b26) 2001; 68 (b32) 2007 Williams, N. M., O'Donovan, M. C., Owen, M. J. (b12) 2006; 73 Wilson, G. M. (b6) 2006; 15 Marshall, C. R. (b8) 2008; 82 Brzustowicz, L. M., Hodgkinson, K. A., Chow, E. W., Honer, W. G., Bassett, A. S. (b25) 2000; 288 Karayiorgou, M. (b19) 1995; 92 Lupski, J. R. (b16) 1998; 14 McCarroll, S. (b13) Sharp, A. J. (b17) 2008; 40 Purcell, S. (b14) 2007; 81 Walsh, T. (b2) 2008; 320 Shaikh, T. H. (b20) 2000; 9 Freedman, R. (b22) 1997; 94 Ross, C. A., Pearlson, G. D. (b18) 1996; 19 Flomen (CR4) 2006; 141 Walsh (CR2) 2008; 320 CR15 Shaikh (CR28) 2007; 17 Lee, Lupski (CR11) 2006; 52 CR13 Brzustowicz, Hodgkinson, Chow, Honer, Bassett (CR25) 2000; 288 CR32 CR31 CR30 Freedman (CR22) 1997; 94 Moon (CR7) 2006; 344 Sharp (CR24) 2006; 38 Wilson (CR6) 2006; 15 Lee, Carvalho, Lupski (CR29) 2007; 131 Gurling (CR26) 2001; 68 Sebat (CR9) 2007; 316 Kirov (CR3) 2008; 17 Ross, Pearlson (CR18) 1996; 19 Butler, Fischer, Kibiryeva, Bittel (CR21) 2008; 146 Lupski (CR16) 1998; 14 Sharp (CR17) 2008; 40 Weiss (CR10) 2008; 358 Sullivan, Kendler, Neale (CR1) 2003; 60 Karayiorgou (CR19) 1995; 92 Xu (CR23) 2001; 105 Stankiewicz, Lupski (CR27) 2002; 18 Marshall (CR8) 2008; 82 Shaikh (CR20) 2000; 9 Friedman (CR5) 2008; 13 Purcell (CR14) 2007; 81 Williams, O’Donovan, Owen (CR12) 2006; 73 21491642 - Nat Rev Genet. 2008 Sep;9(9):654 18784712 - Nature. 2008 Sep 11;455(7210):178-9 BFnature07239_CR32 BFnature07239_CR31 NM Williams (BFnature07239_CR12) 2006; 73 CA Ross (BFnature07239_CR18) 1996; 19 BFnature07239_CR30 LA Weiss (BFnature07239_CR10) 2008; 358 G Kirov (BFnature07239_CR3) 2008; 17 GM Wilson (BFnature07239_CR6) 2006; 15 CR Marshall (BFnature07239_CR8) 2008; 82 BFnature07239_CR15 T Walsh (BFnature07239_CR2) 2008; 320 BFnature07239_CR13 M Karayiorgou (BFnature07239_CR19) 1995; 92 MG Butler (BFnature07239_CR21) 2008; 146 TH Shaikh (BFnature07239_CR20) 2000; 9 AJ Sharp (BFnature07239_CR24) 2006; 38 JA Lee (BFnature07239_CR29) 2007; 131 PF Sullivan (BFnature07239_CR1) 2003; 60 JR Lupski (BFnature07239_CR16) 1998; 14 AJ Sharp (BFnature07239_CR17) 2008; 40 J Sebat (BFnature07239_CR9) 2007; 316 S Purcell (BFnature07239_CR14) 2007; 81 J Xu (BFnature07239_CR23) 2001; 105 LM Brzustowicz (BFnature07239_CR25) 2000; 288 JA Lee (BFnature07239_CR11) 2006; 52 RH Flomen (BFnature07239_CR4) 2006; 141 JI Friedman (BFnature07239_CR5) 2008; 13 R Freedman (BFnature07239_CR22) 1997; 94 P Stankiewicz (BFnature07239_CR27) 2002; 18 HJ Moon (BFnature07239_CR7) 2006; 344 TH Shaikh (BFnature07239_CR28) 2007; 17 HM Gurling (BFnature07239_CR26) 2001; 68 |
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Snippet | Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73-90% (ref. 1).... The genetics of schizophrenia The genetics of schizophrenia and other mental disorders are complex and poorly understood, and made even harder to study because... Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73-90%.... Schizophrenia is a severe mental disorder marked by hallucinations, delusions, cognitive deficits and apathy, with a heritability estimated at 73 - 90% ( ref.... |
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SubjectTerms | Adult and adolescent clinical studies Biological and medical sciences Case-Control Studies Chromosome Deletion Chromosomes Chromosomes, Human - genetics Colleges & universities Gene Dosage - genetics Gene Duplication Genes Genetic aspects Genetic Predisposition to Disease - genetics Genetic variance Genetic variation Genome, Human - genetics Humanities and Social Sciences Humans Intellectual disabilities letter Medical sciences MEDICIN Medicin och hälsovetenskap MEDICINE Mental disorders Models, Genetic multidisciplinary Oligonucleotide Array Sequence Analysis Polymorphism, Single Nucleotide - genetics Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Risk factors Schizophrenia Schizophrenia - genetics Science Science (multidisciplinary) Sequence Deletion - genetics |
Title | Rare chromosomal deletions and duplications increase risk of schizophrenia |
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