The interaction between BDNF and DRD2 in Bipolar II disorder but not in bipolar i disorder
Identifieur interne : 001839 ( Istex/Corpus ); précédent : 001838; suivant : 001840The interaction between BDNF and DRD2 in Bipolar II disorder but not in bipolar i disorder
Auteurs : Chih-Chun Huang ; Yun-Hsuan Chang ; Sheng-Yu Lee ; Shiou-Lan Chen ; Shih-Heng Chen ; Chun-Hsien Chu ; San-Yuan Huang ; Nian-Sheng Tzeng ; I Hui Lee ; Tzung Lieh Yeh ; Yen Kuang Yang ; Ru-Band LuSource :
- American Journal of Medical Genetics Part B: Neuropsychiatric Genetics [ 1552-4841 ] ; 2012-07.
English descriptors
- KwdEn :
Abstract
Bipolar I (BP‐I) and bipolar II (BP‐II) disorders are the two most common subtypes of bipolar disorder. However, most studies have not differentiated bipolar disorder into BP‐I and BP‐II groups, for which the underlying etiology differentiating these two subtypes remains unclear. The genetic association between both subtypes is essential for improving our understanding. The dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1), one of the dopaminergic pathways, as well as the brain‐derived neurotrophic factor (BDNF) gene, were reported as candidate genes in the etiology of bipolar disorder. Therefore, we examined the contribution of the BDNF and DRD2/ANKK1 genes and their interaction to the differentiation of BP‐I and BP‐II. Seven hundred ninety‐two participants were recruited: 208 with BP‐I, 329 with BP‐II, and 255 healthy controls. The genotypes of the BDNF and DRD2/ANKK1 Taq1A polymorphisms were determined using polymerase chain reactions plus restriction fragment length polymorphism analysis. A significant main effect for the Val/Val genotype of the BDNF Val66Met polymorphism predicted BP‐II patients. The significant interaction effect for the Val/Val genotype of the BDNF Val66Met polymorphism and A1/A2 genotype of DRD2/ANKK1 Taq1A polymorphism was found only in BP‐II patients. We provide initial evidence that the BDNF Val66Me and DRD2/ANKK1 Taq1A polymorphisms interact only in BP‐II disorder and that BP‐I and BP‐II are genetically distinct. © 2012 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/ajmg.b.32055
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<front><div type="abstract" xml:lang="en">Bipolar I (BP‐I) and bipolar II (BP‐II) disorders are the two most common subtypes of bipolar disorder. However, most studies have not differentiated bipolar disorder into BP‐I and BP‐II groups, for which the underlying etiology differentiating these two subtypes remains unclear. The genetic association between both subtypes is essential for improving our understanding. The dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1), one of the dopaminergic pathways, as well as the brain‐derived neurotrophic factor (BDNF) gene, were reported as candidate genes in the etiology of bipolar disorder. Therefore, we examined the contribution of the BDNF and DRD2/ANKK1 genes and their interaction to the differentiation of BP‐I and BP‐II. Seven hundred ninety‐two participants were recruited: 208 with BP‐I, 329 with BP‐II, and 255 healthy controls. The genotypes of the BDNF and DRD2/ANKK1 Taq1A polymorphisms were determined using polymerase chain reactions plus restriction fragment length polymorphism analysis. A significant main effect for the Val/Val genotype of the BDNF Val66Met polymorphism predicted BP‐II patients. The significant interaction effect for the Val/Val genotype of the BDNF Val66Met polymorphism and A1/A2 genotype of DRD2/ANKK1 Taq1A polymorphism was found only in BP‐II patients. We provide initial evidence that the BDNF Val66Me and DRD2/ANKK1 Taq1A polymorphisms interact only in BP‐II disorder and that BP‐I and BP‐II are genetically distinct. © 2012 Wiley Periodicals, Inc.</div>
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<abstract>Bipolar I (BP‐I) and bipolar II (BP‐II) disorders are the two most common subtypes of bipolar disorder. However, most studies have not differentiated bipolar disorder into BP‐I and BP‐II groups, for which the underlying etiology differentiating these two subtypes remains unclear. The genetic association between both subtypes is essential for improving our understanding. The dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1), one of the dopaminergic pathways, as well as the brain‐derived neurotrophic factor (BDNF) gene, were reported as candidate genes in the etiology of bipolar disorder. Therefore, we examined the contribution of the BDNF and DRD2/ANKK1 genes and their interaction to the differentiation of BP‐I and BP‐II. Seven hundred ninety‐two participants were recruited: 208 with BP‐I, 329 with BP‐II, and 255 healthy controls. The genotypes of the BDNF and DRD2/ANKK1 Taq1A polymorphisms were determined using polymerase chain reactions plus restriction fragment length polymorphism analysis. A significant main effect for the Val/Val genotype of the BDNF Val66Met polymorphism predicted BP‐II patients. The significant interaction effect for the Val/Val genotype of the BDNF Val66Met polymorphism and A1/A2 genotype of DRD2/ANKK1 Taq1A polymorphism was found only in BP‐II patients. We provide initial evidence that the BDNF Val66Me and DRD2/ANKK1 Taq1A polymorphisms interact only in BP‐II disorder and that BP‐I and BP‐II are genetically distinct. © 2012 Wiley Periodicals, Inc.</abstract>
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<notesStmt><note type="content">*Conflicts of interest: The authors of this paper do not have any commercial associations that might pose a conflict of interest in connection with this manuscript.</note>
<note type="content">*How to Cite this Article: Huang C‐C, Chang Y‐H, Lee S‐Y, Chen S‐L, Chen S‐H, Chu C‐H, Huang S‐Y, Tzeng N‐S, Lee IH, Yeh TL, Yang YK, Lu R‐B. 2012. The Interaction Between BDNF and DRD2 in Bipolar II Disorder but not in Bipolar I Disorder. Am J Med Genet Part B 159B:501–507.</note>
<note>Taiwan National Health Research Institute - No. NHRI‐EX99‐9738NI;</note>
<note>Taiwan National Science Council - No. NSC98‐2627‐B‐006‐017; No. NSC99‐2627‐B‐006‐015;</note>
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<abstract xml:lang="en"><p>Bipolar I (BP‐I) and bipolar II (BP‐II) disorders are the two most common subtypes of bipolar disorder. However, most studies have not differentiated bipolar disorder into BP‐I and BP‐II groups, for which the underlying etiology differentiating these two subtypes remains unclear. The genetic association between both subtypes is essential for improving our understanding. The dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1), one of the dopaminergic pathways, as well as the brain‐derived neurotrophic factor (BDNF) gene, were reported as candidate genes in the etiology of bipolar disorder. Therefore, we examined the contribution of the BDNF and DRD2/ANKK1 genes and their interaction to the differentiation of BP‐I and BP‐II. Seven hundred ninety‐two participants were recruited: 208 with BP‐I, 329 with BP‐II, and 255 healthy controls. The genotypes of the BDNF and DRD2/ANKK1 Taq1A polymorphisms were determined using polymerase chain reactions plus restriction fragment length polymorphism analysis. A significant main effect for the Val/Val genotype of the BDNF Val66Met polymorphism predicted BP‐II patients. The significant interaction effect for the Val/Val genotype of the BDNF Val66Met polymorphism and A1/A2 genotype of DRD2/ANKK1 Taq1A polymorphism was found only in BP‐II patients. We provide initial evidence that the BDNF Val66Me and DRD2/ANKK1 Taq1A polymorphisms interact only in BP‐II disorder and that BP‐I and BP‐II are genetically distinct. © 2012 Wiley Periodicals, Inc.</p>
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<p>Bipolar I (BP‐I) and bipolar II (BP‐II) disorders are the two most common subtypes of bipolar disorder. However, most studies have not differentiated bipolar disorder into BP‐I and BP‐II groups, for which the underlying etiology differentiating these two subtypes remains unclear. The genetic association between both subtypes is essential for improving our understanding. The dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (<i>DRD2/ANKK1</i>
), one of the dopaminergic pathways, as well as the brain‐derived neurotrophic factor (<i>BDNF</i>
) gene, were reported as candidate genes in the etiology of bipolar disorder. Therefore, we examined the contribution of the <i>BDNF</i>
and <i>DRD2/ANKK1</i>
genes and their interaction to the differentiation of BP‐I and BP‐II. Seven hundred ninety‐two participants were recruited: 208 with BP‐I, 329 with BP‐II, and 255 healthy controls. The genotypes of the <i>BDNF</i>
and <i>DRD2/ANKK1 Taq1A</i>
polymorphisms were determined using polymerase chain reactions plus restriction fragment length polymorphism analysis. A significant main effect for the Val/Val genotype of the <i>BDNF</i>
Val66Met polymorphism predicted BP‐II patients. The significant interaction effect for the Val/Val genotype of the <i>BDNF</i>
Val66Met polymorphism and A1/A2 genotype of <i>DRD2/ANKK1 Taq1A</i>
polymorphism was found only in BP‐II patients. We provide initial evidence that the <i>BDNF</i>
Val66Me and <i>DRD2/ANKK1 Taq1A</i>
polymorphisms interact only in BP‐II disorder and that BP‐I and BP‐II are genetically distinct. © 2012 Wiley Periodicals, Inc.</p>
</abstract>
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<noteGroup><note xml:id="fn1"><p>Conflicts of interest: The authors of this paper do not have any commercial associations that might pose a conflict of interest in connection with this manuscript.</p>
</note>
<note xml:id="fn2"><p>How to Cite this Article: Huang C‐C, Chang Y‐H, Lee S‐Y, Chen S‐L, Chen S‐H, Chu C‐H, Huang S‐Y, Tzeng N‐S, Lee IH, Yeh TL, Yang YK, Lu R‐B. 2012. The Interaction Between BDNF and DRD2 in Bipolar II Disorder but not in Bipolar I Disorder. Am J Med Genet Part B 159B:501–507.</p>
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<mods version="3.6"><titleInfo lang="en"><title>The interaction between BDNF and DRD2 in Bipolar II disorder but not in bipolar i disorder</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en"><title>The interaction between BDNF and DRD2 in Bipolar II disorder but not in bipolar i disorder</title>
</titleInfo>
<name type="personal"><namePart type="given">Chih‐Chun</namePart>
<namePart type="family">Huang</namePart>
<affiliation>Department of Medicine, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<affiliation>Department of Psychiatry, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Yun‐Hsuan</namePart>
<namePart type="family">Chang</namePart>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Division of Clinical Psychology, Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Sheng‐Yu</namePart>
<namePart type="family">Lee</namePart>
<affiliation>Department of Psychiatry, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Shiou‐Lan</namePart>
<namePart type="family">Chen</namePart>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Shih‐Heng</namePart>
<namePart type="family">Chen</namePart>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Chun‐Hsien</namePart>
<namePart type="family">Chu</namePart>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">San‐Yuan</namePart>
<namePart type="family">Huang</namePart>
<affiliation>Department of Psychiatry, Tri‐Service General Hospital, National Defense Medical Center, Taipei, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Nian‐Sheng</namePart>
<namePart type="family">Tzeng</namePart>
<affiliation>Department of Psychiatry, Tri‐Service General Hospital, National Defense Medical Center, Taipei, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">I Hui</namePart>
<namePart type="family">Lee</namePart>
<affiliation>Department of Psychiatry, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Tzung Lieh</namePart>
<namePart type="family">Yeh</namePart>
<affiliation>Department of Psychiatry, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Yen Kuang</namePart>
<namePart type="family">Yang</namePart>
<affiliation>Department of Psychiatry, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Addiction Research Center, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Ru‐Band</namePart>
<namePart type="family">Lu</namePart>
<affiliation>Department of Medicine, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<affiliation>Department of Psychiatry, National Cheng Kung University Hospital, Tainan, Taiwan</affiliation>
<affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Division of Clinical Psychology, Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Addiction Research Center, College of Medicine, National Cheng Kung University, Tainan, Taiwan</affiliation>
<affiliation>Institute of Behavioral Medicine, Institute of Allied Health Sciences, Department of Psychiatry College of Medicine and Hospital, National Cheng Kung University 138 Sheng‐Li Road, Tainan 70428, Taiwan.</affiliation>
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<dateIssued encoding="w3cdtf">2012-07</dateIssued>
<dateCaptured encoding="w3cdtf">2011-10-04</dateCaptured>
<dateValid encoding="w3cdtf">2012-04-04</dateValid>
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<abstract lang="en">Bipolar I (BP‐I) and bipolar II (BP‐II) disorders are the two most common subtypes of bipolar disorder. However, most studies have not differentiated bipolar disorder into BP‐I and BP‐II groups, for which the underlying etiology differentiating these two subtypes remains unclear. The genetic association between both subtypes is essential for improving our understanding. The dopamine D2 receptor/ankyrin repeat and kinase domain containing 1 (DRD2/ANKK1), one of the dopaminergic pathways, as well as the brain‐derived neurotrophic factor (BDNF) gene, were reported as candidate genes in the etiology of bipolar disorder. Therefore, we examined the contribution of the BDNF and DRD2/ANKK1 genes and their interaction to the differentiation of BP‐I and BP‐II. Seven hundred ninety‐two participants were recruited: 208 with BP‐I, 329 with BP‐II, and 255 healthy controls. The genotypes of the BDNF and DRD2/ANKK1 Taq1A polymorphisms were determined using polymerase chain reactions plus restriction fragment length polymorphism analysis. A significant main effect for the Val/Val genotype of the BDNF Val66Met polymorphism predicted BP‐II patients. The significant interaction effect for the Val/Val genotype of the BDNF Val66Met polymorphism and A1/A2 genotype of DRD2/ANKK1 Taq1A polymorphism was found only in BP‐II patients. We provide initial evidence that the BDNF Val66Me and DRD2/ANKK1 Taq1A polymorphisms interact only in BP‐II disorder and that BP‐I and BP‐II are genetically distinct. © 2012 Wiley Periodicals, Inc.</abstract>
<note type="content">*Conflicts of interest: The authors of this paper do not have any commercial associations that might pose a conflict of interest in connection with this manuscript.</note>
<note type="content">*How to Cite this Article: Huang C‐C, Chang Y‐H, Lee S‐Y, Chen S‐L, Chen S‐H, Chu C‐H, Huang S‐Y, Tzeng N‐S, Lee IH, Yeh TL, Yang YK, Lu R‐B. 2012. The Interaction Between BDNF and DRD2 in Bipolar II Disorder but not in Bipolar I Disorder. Am J Med Genet Part B 159B:501–507.</note>
<note type="funding">Taiwan National Health Research Institute - No. NHRI‐EX99‐9738NI; </note>
<note type="funding">Taiwan National Science Council - No. NSC98‐2627‐B‐006‐017; No. NSC99‐2627‐B‐006‐015; </note>
<note type="funding">National Cheng Kung University Project</note>
<subject lang="en"><genre>keywords</genre>
<topic>BDNF</topic>
<topic>bipolar disorders</topic>
<topic>DRD2/ANKK1</topic>
<topic>genetic interaction</topic>
</subject>
<relatedItem type="host"><titleInfo><title>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</title>
</titleInfo>
<titleInfo type="abbreviated"><title>Am. J. Med. Genet.</title>
</titleInfo>
<genre type="journal">journal</genre>
<subject><genre>article-category</genre>
<topic>Research Article</topic>
</subject>
<identifier type="ISSN">1552-4841</identifier>
<identifier type="eISSN">1552-485X</identifier>
<identifier type="DOI">10.1002/(ISSN)1552-485X</identifier>
<identifier type="PublisherID">AJMG</identifier>
<part><date>2012</date>
<detail type="volume"><caption>vol.</caption>
<number>159B</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>5</number>
</detail>
<extent unit="pages"><start>501</start>
<end>507</end>
<total>7</total>
</extent>
</part>
</relatedItem>
<relatedItem type="preceding"><titleInfo><title>American Journal of Medical Genetics</title>
</titleInfo>
<identifier type="ISSN">0148-7299</identifier>
<identifier type="ISSN">1096-8628</identifier>
<part><date point="end">2004</date>
</part>
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<identifier type="DOI">10.1002/ajmg.b.32055</identifier>
<identifier type="ArticleID">AJMG32055</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2012 Wiley Periodicals, Inc.</accessCondition>
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