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Article: Further evidence for shared genetic effects between psychotic bipolar disorder and P50 suppression: A combined twin and family study

TitleFurther evidence for shared genetic effects between psychotic bipolar disorder and P50 suppression: A combined twin and family study
Authors
KeywordsBipolar disorder
Endophenotype
P50 ERPs
Twin modelling
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0148-7299:1
Citation
American Journal Of Medical Genetics, Part B: Neuropsychiatric Genetics, 2008, v. 147 n. 5, p. 619-627 How to Cite?
AbstractP50 suppression deficit has been reported in patients with psychotic bipolar disorder. In our previous report on twin pairs concordant and discordant for bipolar disorder, we found significant genetic overlap between bipolar disorder and P50 sensory gating. However, the sample size in that study was relatively small. A separate study, the Maudsley Bipolar Family Study, reported diminished P50 gating in unaffected relatives of psychotic bipolar patients. However, genetic and environmental influences are confounded in family studies due to lack of monozygotic (MZ) twin pairs. The current study combines the twin sample and the family sample in order to improve statistical power and study design, with the aims of: (1) substantiating the association between psychotic bipolar disorder and diminished P50 suppression and (2) verifying the genetic overlap between the two traits reported in the twin sample. We also assessed the relationship between bipolar disorder and an alternative suppression index, the P50 Condition-Testing (C-T) amplitude difference. A total of 309 subjects was included in this study, comprising 91 twin pairs, 31 bipolar families, and 45 unrelated healthy controls. Statistical analyses were based on structural equation modeling. Bipolar disorder was significantly associated with a diminished P50 suppression ratio and decreased C-T amplitude difference. Shared genetic factors were the main source of these associations. Suppression impairment was due to larger, poorly gated, T amplitude responses. The results provide further evidence that impaired P50 suppressions are promising endophenotypes for psychotic bipolar disorder. The non-specificity of impaired P50 suppression may reflect the impact of shared psychosis susceptibility genes. © 2008 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/59715
ISSN
2015 SCImago Journal Rankings: 1.771
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHall, MHen_HK
dc.contributor.authorSchulze, Ken_HK
dc.contributor.authorSham, Pen_HK
dc.contributor.authorKalidindi, Sen_HK
dc.contributor.authorMcDonald, Cen_HK
dc.contributor.authorBramon, Een_HK
dc.contributor.authorLevy, DLen_HK
dc.contributor.authorMurray, RMen_HK
dc.contributor.authorRijsdijk, Fen_HK
dc.date.accessioned2010-05-31T03:55:57Z-
dc.date.available2010-05-31T03:55:57Z-
dc.date.issued2008en_HK
dc.identifier.citationAmerican Journal Of Medical Genetics, Part B: Neuropsychiatric Genetics, 2008, v. 147 n. 5, p. 619-627en_HK
dc.identifier.issn1552-485Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/59715-
dc.description.abstractP50 suppression deficit has been reported in patients with psychotic bipolar disorder. In our previous report on twin pairs concordant and discordant for bipolar disorder, we found significant genetic overlap between bipolar disorder and P50 sensory gating. However, the sample size in that study was relatively small. A separate study, the Maudsley Bipolar Family Study, reported diminished P50 gating in unaffected relatives of psychotic bipolar patients. However, genetic and environmental influences are confounded in family studies due to lack of monozygotic (MZ) twin pairs. The current study combines the twin sample and the family sample in order to improve statistical power and study design, with the aims of: (1) substantiating the association between psychotic bipolar disorder and diminished P50 suppression and (2) verifying the genetic overlap between the two traits reported in the twin sample. We also assessed the relationship between bipolar disorder and an alternative suppression index, the P50 Condition-Testing (C-T) amplitude difference. A total of 309 subjects was included in this study, comprising 91 twin pairs, 31 bipolar families, and 45 unrelated healthy controls. Statistical analyses were based on structural equation modeling. Bipolar disorder was significantly associated with a diminished P50 suppression ratio and decreased C-T amplitude difference. Shared genetic factors were the main source of these associations. Suppression impairment was due to larger, poorly gated, T amplitude responses. The results provide further evidence that impaired P50 suppressions are promising endophenotypes for psychotic bipolar disorder. The non-specificity of impaired P50 suppression may reflect the impact of shared psychosis susceptibility genes. © 2008 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0148-7299:1en_HK
dc.relation.ispartofAmerican Journal of Medical Genetics, Part B: Neuropsychiatric Geneticsen_HK
dc.rightsAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectBipolar disorderen_HK
dc.subjectEndophenotypeen_HK
dc.subjectP50 ERPsen_HK
dc.subjectTwin modellingen_HK
dc.titleFurther evidence for shared genetic effects between psychotic bipolar disorder and P50 suppression: A combined twin and family studyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1552-4841&volume=147B&spage=619&epage=627&date=2008&atitle=Further+Evidence+for+Shared+Genetic+Effects+Between+Psychotic+Bipolar+Disorder+and+P50+Suppression:+A+Combined+Twin+and+Family+Studyen_HK
dc.identifier.emailSham, P: pcsham@hku.hken_HK
dc.identifier.authoritySham, P=rp00459en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ajmg.b.30653en_HK
dc.identifier.pmid18189279-
dc.identifier.scopuseid_2-s2.0-46949087544en_HK
dc.identifier.hkuros157975en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-46949087544&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume147en_HK
dc.identifier.issue5en_HK
dc.identifier.spage619en_HK
dc.identifier.epage627en_HK
dc.identifier.isiWOS:000257447000012-
dc.identifier.scopusauthoridHall, MH=14013171900en_HK
dc.identifier.scopusauthoridSchulze, K=7103137549en_HK
dc.identifier.scopusauthoridSham, P=34573429300en_HK
dc.identifier.scopusauthoridKalidindi, S=24366595400en_HK
dc.identifier.scopusauthoridMcDonald, C=8749594800en_HK
dc.identifier.scopusauthoridBramon, E=8089378900en_HK
dc.identifier.scopusauthoridLevy, DL=7402084343en_HK
dc.identifier.scopusauthoridMurray, RM=35406239400en_HK
dc.identifier.scopusauthoridRijsdijk, F=6701830835en_HK

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