Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co‐morbid with alcoholism
Identifieur interne : 001878 ( Istex/Corpus ); précédent : 001877; suivant : 001879Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co‐morbid with alcoholism
Auteurs : Ru-Band Lu ; Jia-Fu Lee ; San-Yuan Huang ; Sheng-Yu Lee ; Yun-Hsuan Chang ; Po-Hsiu Kuo ; Shiou-Lan Chen ; Shih-Heng Chen ; Chun-Hsien Chu ; Wei-Wen Lin ; Pei-Lin Wu ; Huei-Chen KoSource :
- Addiction Biology [ 1355-6215 ] ; 2012-09.
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Abstract
Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or alcoholism because the ALDH2*2 allele protects against the risk of developing alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co‐morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co‐morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without alcoholism (ASPD not co‐morbid with alcohol dependence, antisocial non‐ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non‐ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non‐ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co‐morbid alcoholism.
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DOI: 10.1111/j.1369-1600.2010.00268.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co‐morbid with alcoholism</title><author><name sortKey="Lu, Ru And" sort="Lu, Ru And" uniqKey="Lu R" first="Ru-Band" last="Lu">Ru-Band Lu</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: rblu@mail.ncku.edu.tw</mods:affiliation></affiliation></author><author><name sortKey="Lee, Jia U" sort="Lee, Jia U" uniqKey="Lee J" first="Jia-Fu" last="Lee">Jia-Fu Lee</name><affiliation><mods:affiliation>Armed Forces Pei‐Tou Hospital, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Huang, San Uan" sort="Huang, San Uan" uniqKey="Huang S" first="San-Yuan" last="Huang">San-Yuan Huang</name><affiliation><mods:affiliation>Department of Psychiatry, National Defense Medical Center, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Lee, Sheng U" sort="Lee, Sheng U" uniqKey="Lee S" first="Sheng-Yu" last="Lee">Sheng-Yu Lee</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chang, Yun Suan" sort="Chang, Yun Suan" uniqKey="Chang Y" first="Yun-Hsuan" last="Chang">Yun-Hsuan Chang</name><affiliation><mods:affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Kuo, Po Siu" sort="Kuo, Po Siu" uniqKey="Kuo P" first="Po-Hsiu" last="Kuo">Po-Hsiu Kuo</name><affiliation><mods:affiliation>Graduate Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chen, Shiou An" sort="Chen, Shiou An" uniqKey="Chen S" first="Shiou-Lan" last="Chen">Shiou-Lan Chen</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chen, Shih Eng" sort="Chen, Shih Eng" uniqKey="Chen S" first="Shih-Heng" last="Chen">Shih-Heng Chen</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chu, Chun Sien" sort="Chu, Chun Sien" uniqKey="Chu C" first="Chun-Hsien" last="Chu">Chun-Hsien Chu</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Lin, Wei En" sort="Lin, Wei En" uniqKey="Lin W" first="Wei-Wen" last="Lin">Wei-Wen Lin</name><affiliation><mods:affiliation>Department of Psychiatry, National Defense Medical Center, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Wu, Pei In" sort="Wu, Pei In" uniqKey="Wu P" first="Pei-Lin" 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Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: rblu@mail.ncku.edu.tw</mods:affiliation></affiliation></author><author><name sortKey="Lee, Jia U" sort="Lee, Jia U" uniqKey="Lee J" first="Jia-Fu" last="Lee">Jia-Fu Lee</name><affiliation><mods:affiliation>Armed Forces Pei‐Tou Hospital, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Huang, San Uan" sort="Huang, San Uan" uniqKey="Huang S" first="San-Yuan" last="Huang">San-Yuan Huang</name><affiliation><mods:affiliation>Department of Psychiatry, National Defense Medical Center, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Lee, Sheng U" sort="Lee, Sheng U" uniqKey="Lee S" first="Sheng-Yu" last="Lee">Sheng-Yu Lee</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chang, Yun Suan" sort="Chang, Yun Suan" uniqKey="Chang Y" first="Yun-Hsuan" last="Chang">Yun-Hsuan Chang</name><affiliation><mods:affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Kuo, Po Siu" sort="Kuo, Po Siu" uniqKey="Kuo P" first="Po-Hsiu" last="Kuo">Po-Hsiu Kuo</name><affiliation><mods:affiliation>Graduate Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chen, Shiou An" sort="Chen, Shiou An" uniqKey="Chen S" first="Shiou-Lan" last="Chen">Shiou-Lan Chen</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chen, Shih Eng" sort="Chen, Shih Eng" uniqKey="Chen S" first="Shih-Heng" last="Chen">Shih-Heng Chen</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chu, Chun Sien" sort="Chu, Chun Sien" uniqKey="Chu C" first="Chun-Hsien" last="Chu">Chun-Hsien Chu</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Lin, Wei En" sort="Lin, Wei En" uniqKey="Lin W" first="Wei-Wen" last="Lin">Wei-Wen Lin</name><affiliation><mods:affiliation>Department of Psychiatry, National Defense Medical Center, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Wu, Pei In" sort="Wu, Pei In" uniqKey="Wu P" first="Pei-Lin" last="Wu">Pei-Lin Wu</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Ko, Huei Hen" sort="Ko, Huei Hen" uniqKey="Ko H" first="Huei-Chen" last="Ko">Huei-Chen Ko</name><affiliation><mods:affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Addiction Biology</title><idno type="ISSN">1355-6215</idno><idno type="eISSN">1369-1600</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2012-09">2012-09</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="865">865</biblScope><biblScope unit="page" to="874">874</biblScope></imprint><idno type="ISSN">1355-6215</idno></series><idno type="istex">8A764E3EC7C16440EAC96CB14AD33E4DF535F7FB</idno><idno type="DOI">10.1111/j.1369-1600.2010.00268.x</idno><idno type="ArticleID">ADB268</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1355-6215</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ALDH</term><term>Alcoholism</term><term>DRD2</term><term>antisocial personality disorder</term><term>comorbidity</term><term>gene</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or alcoholism because the ALDH2*2 allele protects against the risk of developing alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co‐morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co‐morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without alcoholism (ASPD not co‐morbid with alcohol dependence, antisocial non‐ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non‐ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non‐ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co‐morbid alcoholism.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ru‐Band Lu</name><affiliations><json:string>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string><json:string>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</json:string><json:string>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</json:string><json:string>E-mail: rblu@mail.ncku.edu.tw</json:string></affiliations></json:item><json:item><name>Jia‐Fu Lee</name><affiliations><json:string>Armed Forces Pei‐Tou Hospital, Taiwan</json:string></affiliations></json:item><json:item><name>San‐Yuan Huang</name><affiliations><json:string>Department of Psychiatry, National Defense Medical Center, Taiwan</json:string></affiliations></json:item><json:item><name>Sheng‐Yu Lee</name><affiliations><json:string>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string><json:string>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item><json:item><name>Yun‐Hsuan Chang</name><affiliations><json:string>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</json:string><json:string>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item><json:item><name>Po‐Hsiu Kuo</name><affiliations><json:string>Graduate Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item><json:item><name>Shiou‐Lan Chen</name><affiliations><json:string>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string><json:string>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item><json:item><name>Shih‐Heng Chen</name><affiliations><json:string>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item><json:item><name>Chun‐Hsien Chu</name><affiliations><json:string>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item><json:item><name>Wei‐Wen Lin</name><affiliations><json:string>Department of Psychiatry, National Defense Medical Center, Taiwan</json:string></affiliations></json:item><json:item><name>Pei‐Lin Wu</name><affiliations><json:string>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item><json:item><name>Huei‐Chen Ko</name><affiliations><json:string>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</json:string><json:string>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Alcoholism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ALDH</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>antisocial personality disorder</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>comorbidity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>DRD2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gene</value></json:item></subject><articleId><json:string>ADB268</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or alcoholism because the ALDH2*2 allele protects against the risk of developing alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co‐morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co‐morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without alcoholism (ASPD not co‐morbid with alcohol dependence, antisocial non‐ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non‐ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non‐ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co‐morbid alcoholism.</abstract><qualityIndicators><score>7.772</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1624</abstractCharCount><pdfWordCount>6988</pdfWordCount><pdfCharCount>44245</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>231</abstractWordCount></qualityIndicators><title>Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co‐morbid with alcoholism</title><refBibs><json:item><author><json:item><name>DP Agarwal</name></json:item><json:item><name>HW Goedde</name></json:item></author><host><volume>2</volume><pages><last>62</last><first>48</first></pages><author></author><title>Pharmacogenetics</title></host><title>Pharmacogenetics of alcohol metabolism and alcoholism</title></json:item><json:item><host><author></author><title>American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorder, 4th edn. 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type="first">Ru‐Band</forename><surname>Lu</surname></persName><email>rblu@mail.ncku.edu.tw</email><affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</affiliation></author><author xml:id="author-2"><persName><forename type="first">Jia‐Fu</forename><surname>Lee</surname></persName><affiliation>Armed Forces Pei‐Tou Hospital, Taiwan</affiliation></author><author xml:id="author-3"><persName><forename type="first">San‐Yuan</forename><surname>Huang</surname></persName><affiliation>Department of Psychiatry, National Defense Medical Center, Taiwan</affiliation></author><author xml:id="author-4"><persName><forename type="first">Sheng‐Yu</forename><surname>Lee</surname></persName><affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</affiliation></author><author xml:id="author-5"><persName><forename type="first">Yun‐Hsuan</forename><surname>Chang</surname></persName><affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</affiliation></author><author xml:id="author-6"><persName><forename type="first">Po‐Hsiu</forename><surname>Kuo</surname></persName><affiliation>Graduate Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation></author><author xml:id="author-7"><persName><forename type="first">Shiou‐Lan</forename><surname>Chen</surname></persName><affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</affiliation></author><author xml:id="author-8"><persName><forename type="first">Shih‐Heng</forename><surname>Chen</surname></persName><affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation></author><author xml:id="author-9"><persName><forename type="first">Chun‐Hsien</forename><surname>Chu</surname></persName><affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation></author><author xml:id="author-10"><persName><forename type="first">Wei‐Wen</forename><surname>Lin</surname></persName><affiliation>Department of Psychiatry, National Defense Medical Center, Taiwan</affiliation></author><author xml:id="author-11"><persName><forename 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The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co‐morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co‐morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without alcoholism (ASPD not co‐morbid with alcohol dependence, antisocial non‐ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non‐ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non‐ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co‐morbid alcoholism.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>Alcoholism</term></item><item><term>ALDH</term></item><item><term>antisocial personality disorder</term></item><item><term>comorbidity</term></item><item><term>DRD2</term></item><item><term>gene</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>HUMAN GENETIC STUDY</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2012-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/8A764E3EC7C16440EAC96CB14AD33E4DF535F7FB/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1369-1600</doi><issn type="print">1355-6215</issn><issn type="electronic">1369-1600</issn><idGroup><id type="product" value="ADB"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ADDICTION BIOLOGY">Addiction Biology</title></titleGroup></publicationMeta><publicationMeta level="part" position="09105"><doi>10.1111/adb.2012.17.issue-5</doi><copyright ownership="thirdParty">© 2012 Society for the Study of Addiction</copyright><numberingGroup><numbering number="17" type="journalVolume">17</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2012-09">September 2012</coverDate></publicationMeta><publicationMeta level="unit" position="30" status="forIssue" type="article"><doi origin="wiley">10.1111/j.1369-1600.2010.00268.x</doi><idGroup><id type="unit" value="ADB268"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">HUMAN GENETIC STUDY</title><title type="articleCategory">HUMAN GENETIC STUDY</title></titleGroup><copyright>© 2010 The Authors, Addiction Biology © 2010 Society for the Study of Addiction</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:3.1.6 mode:FullText" date="2012-09-12"></event><event date="2012-09-12" type="xmlCorrected"></event><event type="publishedOnlineEarlyUnpaginated" date="2010-11-11"></event><event type="publishedOnlineFinalForm" date="2012-09-14"></event><event type="firstOnline" date="2010-11-11"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2013-12-31"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.3.4 mode:FullText" date="2015-02-25"></event></eventGroup><numberingGroup><numbering type="pageFirst">865</numbering><numbering type="pageLast">874</numbering></numberingGroup><correspondenceTo>Ru‐Band Lu, Institute of Behavioral Medicine, Department of Psychiatry, College of Medicine and Hospital, National Cheng Kung University, 138 Sheng‐Li Road, Tainan 70428, Taiwan. E‐mail: <email>rblu@mail.ncku.edu.tw</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ADB.ADB268.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="54"></count><count type="wordTotal" number="7702"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Interaction between <i>ALDH2</i>*<i>1</i>*<i>1</i> and <i>DRD2/ANKK1 TaqI A1A1</i> genes may be associated with antisocial personality disorder not co‐morbid with alcoholism</title><title type="shortAuthors">Ru‐Band Lu et al.</title><title type="short">Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2 #a3" corresponding="yes"><personName><givenNames>Ru‐Band</givenNames><familyName>Lu</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a4"><personName><givenNames>Jia‐Fu</givenNames><familyName>Lee</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a5"><personName><givenNames>San‐Yuan</givenNames><familyName>Huang</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1 #a2"><personName><givenNames>Sheng‐Yu</givenNames><familyName>Lee</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a2 #a3"><personName><givenNames>Yun‐Hsuan</givenNames><familyName>Chang</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a6"><personName><givenNames>Po‐Hsiu</givenNames><familyName>Kuo</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1 #a2"><personName><givenNames>Shiou‐Lan</givenNames><familyName>Chen</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>Shih‐Heng</givenNames><familyName>Chen</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1"><personName><givenNames>Chun‐Hsien</givenNames><familyName>Chu</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a5"><personName><givenNames>Wei‐Wen</givenNames><familyName>Lin</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a1"><personName><givenNames>Pei‐Lin</givenNames><familyName>Wu</familyName></personName></creator><creator creatorRole="author" xml:id="cr12" affiliationRef="#a1 #a3"><personName><givenNames>Huei‐Chen</givenNames><familyName>Ko</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>Armed Forces Pei‐Tou Hospital, Taiwan</unparsedAffiliation></affiliation><affiliation xml:id="a5"><unparsedAffiliation>Department of Psychiatry, National Defense Medical Center, Taiwan</unparsedAffiliation></affiliation><affiliation xml:id="a6"><unparsedAffiliation>Graduate Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Taiwan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Alcoholism</keyword><keyword xml:id="k2"><i>ALDH</i></keyword><keyword xml:id="k3">antisocial personality disorder</keyword><keyword xml:id="k4">comorbidity</keyword><keyword xml:id="k5"><i>DRD2</i></keyword><keyword xml:id="k6">gene</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">ABSTRACT</title><p>Previous studies on <i>acetaldehyde dehydrogenase</i> 2 (<i>ALDH2</i>) focused on drinking behavior or alcoholism because the <i>ALDH</i>2*<i>2</i> allele protects against the risk of developing alcoholism. The mechanism provides that the <i>ALDH2</i> gene's protective effect is also involved in dopamine metabolism. The interaction of the <i>ALDH2</i> gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co‐morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the <i>ALDH2</i>*<i>1</i>*<i>1</i>, *<i>1</i>*<i>2</i> or *<i>2</i>*<i>2</i> polymorphisms with the <i>dopamine 2 receptor</i> (<i>DRD2</i>) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co‐morbid with alcohol dependence, antisocial ALC; <i>n</i> = 133), ASPD without alcoholism (ASPD not co‐morbid with alcohol dependence, antisocial non‐ALC; <i>n</i> = 164) and community controls (healthy volunteers from the community; <i>n</i> = 244). Compared with healthy controls, individuals with the <i>DRD2 A1/A1</i> and the <i>ALDH2</i>*<i>1/</i>*<i>1</i> genotypes were at a 5.39 times greater risk for antisocial non‐ALC than were those with other genotypes. Our results suggest that the <i>DRD2/ANKK1</i> and <i>ALDH2</i> genes interacted in the antisocial non‐ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co‐morbid alcoholism.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co‐morbid with alcoholism</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co‐morbid with alcoholism</title></titleInfo><name type="personal"><namePart type="given">Ru‐Band</namePart><namePart type="family">Lu</namePart><affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>E-mail: rblu@mail.ncku.edu.tw</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jia‐Fu</namePart><namePart type="family">Lee</namePart><affiliation>Armed Forces Pei‐Tou Hospital, 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, National Defense Medical Center, 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>Institute of Behavioral Medicine, 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type="given">Shiou‐Lan</namePart><namePart type="family">Chen</namePart><affiliation>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation><affiliation>Department of Psychiatry, College of Medicine, National Cheng Kung University, 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>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, 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>Institute of Behavioral Medicine, College of Medicine, National Cheng Kung University, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart 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displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2012-09</dateIssued><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="tables">3</extent><extent unit="references">54</extent><extent unit="words">7702</extent></physicalDescription><abstract lang="en">Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or alcoholism because the ALDH2*2 allele protects against the risk of developing alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co‐morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co‐morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without alcoholism (ASPD not co‐morbid with alcohol dependence, antisocial non‐ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non‐ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non‐ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co‐morbid alcoholism.</abstract><subject lang="en"><genre>keywords</genre><topic>Alcoholism</topic><topic>ALDH</topic><topic>antisocial personality disorder</topic><topic>comorbidity</topic><topic>DRD2</topic><topic>gene</topic></subject><relatedItem type="host"><titleInfo><title>Addiction Biology</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>HUMAN GENETIC STUDY</topic></subject><identifier type="ISSN">1355-6215</identifier><identifier type="eISSN">1369-1600</identifier><identifier type="DOI">10.1111/(ISSN)1369-1600</identifier><identifier type="PublisherID">ADB</identifier><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>865</start><end>874</end><total>10</total></extent></part></relatedItem><identifier type="istex">8A764E3EC7C16440EAC96CB14AD33E4DF535F7FB</identifier><identifier type="DOI">10.1111/j.1369-1600.2010.00268.x</identifier><identifier type="ArticleID">ADB268</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2012 Society for the Study of Addiction© 2010 The Authors, Addiction Biology © 2010 Society for the Study of Addiction</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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