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Article: Genomewide association scan of suicidal thoughts and behaviour in major depression
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TitleGenomewide association scan of suicidal thoughts and behaviour in major depression
 
AuthorsSchosser, A1 13
Butler, AW1 5
Ising, M8
Perroud, N1 14
Uher, R1
Ng, MY1
Cohen-Woods, S1
Craddock, N10
Owen, MJ10
Korszun, A7
Jones, L11
Jones, I10
Gill, M16
Rice, JP3
Maier, W2
Mors, O17
Rietschel, M9
Lucae, S8
Binder, EB8
Preisig, M18
Perry, J6
Tozzi, F6
Muglia, P6 12 15
Aitchison, KJ1
Breen, G1 4
Craig, IW1
Farmer, AE1
Mulller-Myhsok, B
McGuffin, P1
Lewis, CM1
 
Issue Date2011
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPLoS One, 2011, v. 6 n. 7, article no. e20690 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0020690
 
AbstractBACKGROUND: Suicidal behaviour can be conceptualised as a continuum from suicidal ideation, to suicidal attempts to completed suicide. In this study we identify genes contributing to suicidal behaviour in the depression study RADIANT. METHODOLOGY/PRINCIPAL FINDINGS: A quantitative suicidality score was composed of two items from the SCAN interview. In addition, the 251 depression cases with a history of serious suicide attempts were classified to form a discrete trait. The quantitative trait was correlated with younger onset of depression and number of episodes of depression, but not with gender. A genome-wide association study of 2,023 depression cases was performed to identify genes that may contribute to suicidal behaviour. Two Munich depression studies were used as replication cohorts to test the most strongly associated SNPs. No SNP was associated at genome-wide significance level. For the quantitative trait, evidence of association was detected at GFRA1, a receptor for the neurotrophin GDRA (p = 2e-06). For the discrete trait of suicide attempt, SNPs in KIAA1244 and RGS18 attained p-values of <5e-6. None of these SNPs showed evidence for replication in the additional cohorts tested. Candidate gene analysis provided some support for a polymorphism in NTRK2, which was previously associated with suicidality. CONCLUSIONS/SIGNIFICANCE: This study provides a genome-wide assessment of possible genetic contribution to suicidal behaviour in depression but indicates a genetic architecture of multiple genes with small effects. Large cohorts will be required to dissect this further.
 
ISSN1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0020690
 
PubMed Central IDPMC3130038
 
DC FieldValue
dc.contributor.authorSchosser, A
 
dc.contributor.authorButler, AW
 
dc.contributor.authorIsing, M
 
dc.contributor.authorPerroud, N
 
dc.contributor.authorUher, R
 
dc.contributor.authorNg, MY
 
dc.contributor.authorCohen-Woods, S
 
dc.contributor.authorCraddock, N
 
dc.contributor.authorOwen, MJ
 
dc.contributor.authorKorszun, A
 
dc.contributor.authorJones, L
 
dc.contributor.authorJones, I
 
dc.contributor.authorGill, M
 
dc.contributor.authorRice, JP
 
dc.contributor.authorMaier, W
 
dc.contributor.authorMors, O
 
dc.contributor.authorRietschel, M
 
dc.contributor.authorLucae, S
 
dc.contributor.authorBinder, EB
 
dc.contributor.authorPreisig, M
 
dc.contributor.authorPerry, J
 
dc.contributor.authorTozzi, F
 
dc.contributor.authorMuglia, P
 
dc.contributor.authorAitchison, KJ
 
dc.contributor.authorBreen, G
 
dc.contributor.authorCraig, IW
 
dc.contributor.authorFarmer, AE
 
dc.contributor.authorMulller-Myhsok, B
 
dc.contributor.authorMcGuffin, P
 
dc.contributor.authorLewis, CM
 
dc.date.accessioned2012-09-20T08:06:04Z
 
dc.date.available2012-09-20T08:06:04Z
 
dc.date.issued2011
 
dc.description.abstractBACKGROUND: Suicidal behaviour can be conceptualised as a continuum from suicidal ideation, to suicidal attempts to completed suicide. In this study we identify genes contributing to suicidal behaviour in the depression study RADIANT. METHODOLOGY/PRINCIPAL FINDINGS: A quantitative suicidality score was composed of two items from the SCAN interview. In addition, the 251 depression cases with a history of serious suicide attempts were classified to form a discrete trait. The quantitative trait was correlated with younger onset of depression and number of episodes of depression, but not with gender. A genome-wide association study of 2,023 depression cases was performed to identify genes that may contribute to suicidal behaviour. Two Munich depression studies were used as replication cohorts to test the most strongly associated SNPs. No SNP was associated at genome-wide significance level. For the quantitative trait, evidence of association was detected at GFRA1, a receptor for the neurotrophin GDRA (p = 2e-06). For the discrete trait of suicide attempt, SNPs in KIAA1244 and RGS18 attained p-values of <5e-6. None of these SNPs showed evidence for replication in the additional cohorts tested. Candidate gene analysis provided some support for a polymorphism in NTRK2, which was previously associated with suicidality. CONCLUSIONS/SIGNIFICANCE: This study provides a genome-wide assessment of possible genetic contribution to suicidal behaviour in depression but indicates a genetic architecture of multiple genes with small effects. Large cohorts will be required to dissect this further.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPLoS One, 2011, v. 6 n. 7, article no. e20690 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0020690
 
dc.identifier.citeulike9595180
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0020690
 
dc.identifier.hkuros210464
 
dc.identifier.issn1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
dc.identifier.issue7, article no. e20690
 
dc.identifier.pmcidPMC3130038
 
dc.identifier.pmid21750702
 
dc.identifier.scopuseid_2-s2.0-79959981469
 
dc.identifier.urihttp://hdl.handle.net/10722/164567
 
dc.identifier.volume6
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS One
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshAlleles
 
dc.subject.meshDepressive Disorder, Major - genetics - psychology
 
dc.subject.meshGenome-Wide Association Study - methods
 
dc.subject.meshSuicidal Ideation
 
dc.subject.meshSuicide, Attempted
 
dc.titleGenomewide association scan of suicidal thoughts and behaviour in major depression
 
dc.typeArticle
 
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<contributor.author>Perroud, N</contributor.author>
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<contributor.author>Mulller-Myhsok, B</contributor.author>
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<description.abstract>BACKGROUND: Suicidal behaviour can be conceptualised as a continuum from suicidal ideation, to suicidal attempts to completed suicide. In this study we identify genes contributing to suicidal behaviour in the depression study RADIANT. METHODOLOGY/PRINCIPAL FINDINGS: A quantitative suicidality score was composed of two items from the SCAN interview. In addition, the 251 depression cases with a history of serious suicide attempts were classified to form a discrete trait. The quantitative trait was correlated with younger onset of depression and number of episodes of depression, but not with gender. A genome-wide association study of 2,023 depression cases was performed to identify genes that may contribute to suicidal behaviour. Two Munich depression studies were used as replication cohorts to test the most strongly associated SNPs. No SNP was associated at genome-wide significance level. For the quantitative trait, evidence of association was detected at GFRA1, a receptor for the neurotrophin GDRA (p = 2e-06). For the discrete trait of suicide attempt, SNPs in KIAA1244 and RGS18 attained p-values of &lt;5e-6. None of these SNPs showed evidence for replication in the additional cohorts tested. Candidate gene analysis provided some support for a polymorphism in NTRK2, which was previously associated with suicidality. CONCLUSIONS/SIGNIFICANCE: This study provides a genome-wide assessment of possible genetic contribution to suicidal behaviour in depression but indicates a genetic architecture of multiple genes with small effects. Large cohorts will be required to dissect this further.</description.abstract>
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Author Affiliations
  1. King's College London
  2. Universität Bonn
  3. Washington University in St. Louis
  4. South London and Maudsley NHS Foundation Trust
  5. The University of Hong Kong
  6. GlaxoSmithKline
  7. null
  8. Max-Planck-Institut für Psychiatrie
  9. Zentralinstitut für Seelische Gesundheit
  10. Cardiff University
  11. University of Birmingham
  12. Neurosearch AS
  13. Medizinische Universitat Wien
  14. Université de Genève
  15. University of Toronto
  16. Trinity Centre for Health Science
  17. Ârhus Universitetshospital
  18. Universität Lausanne Schweiz