Common and rare alleles of the serotonin transporter gene, SLC6A4, associated with Tourette's disorder.
Identifieur interne : 000929 ( PubMed/Curation ); précédent : 000928; suivant : 000930Common and rare alleles of the serotonin transporter gene, SLC6A4, associated with Tourette's disorder.
Auteurs : Pablo R. Moya [États-Unis] ; Jens R. Wendland ; Liza M. Rubenstein ; Kiara R. Timpano ; Gary A. Heiman ; Jay A. Tischfield ; Robert A. King ; Anne M. Andrews ; Samanda Ramamoorthy ; Francis J. Mcmahon ; Dennis L. MurphySource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Female, Gene Frequency, Genetic Association Studies, Genetic Predisposition to Disease (genetics), Genotype, Humans, Male, Obsessive-Compulsive Disorder (genetics), Polymorphism, Single Nucleotide (genetics), Psychiatric Status Rating Scales, Serotonin Plasma Membrane Transport Proteins (genetics), Tourette Syndrome (genetics).
- MESH :
- chemical , genetics : Serotonin Plasma Membrane Transport Proteins.
- genetics : Genetic Predisposition to Disease, Obsessive-Compulsive Disorder, Polymorphism, Single Nucleotide, Tourette Syndrome.
- Female, Gene Frequency, Genetic Association Studies, Genotype, Humans, Male, Psychiatric Status Rating Scales.
Abstract
To evaluate the hypothesis that functionally over-expressing alleles of the serotonin transporter (SERT) gene (solute carrier family 6, member 4, SLC6A4) are present in Tourette's disorder (TD), just as we previously observed in obsessive compulsive disorder (OCD), we evaluated TD probands (N = 151) and controls (N = 858). We genotyped the refined SERT-linked polymorphic region 5-HTTLPR/rs25531 and the associated rs25532 variant in the SLC6A4 promoter plus the rare coding variant SERT isoleucine-to-valine at position 425 (I425V). The higher expressing 5-HTTLPR/rs25531 LA allele was more prevalent in TD probands than in controls (χ(2) = 5.75; P = 0.017; odds ratio [OR], 1.35); and, in a secondary analysis, surprisingly, it was significantly more frequent in probands who had TD alone than in those who had TD plus OCD (Fisher's exact test; P = 0.0006; OR, 2.29). Likewise, the higher expressing LAC haplotype (5-HTTLPR/rs25531/rs25532) was more frequent in TD probands than in controls (P = 0.024; OR, 1.33) and also in the TD alone group versus the TD plus OCD group (P = 0.0013; OR, 2.14). Furthermore, the rare gain-of-function SERT I425V variant was observed in 3 male siblings with TD and/or OCD and in their father. Thus, the cumulative count of SERT I425V becomes 1.57% in OCD/TD spectrum conditions versus 0.15% in controls, with a recalculated, family-adjusted significance of χ(2) = 15.03 (P < 0.0001; OR, 9.0; total worldwide genotyped, 2914). This report provides a unique combination of common and rare variants in one gene in TD, all of which are associated with SERT gain of function. Thus, altered SERT activity represents a potential contributor to serotonergic abnormalities in TD. The present results call for replication in a similarly intensively evaluated sample. © 2013 Movement Disorder Society.
DOI: 10.1002/mds.25460
PubMed: 23630162
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Moya</name><affiliation wicri:level="1"><nlm:affiliation>National Institute of Mental Health-Intramural Research Program, Bethesda, MD, USA. moyap@mail.nih.gov</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>National Institute of Mental Health-Intramural Research Program, Bethesda, MD</wicri:regionArea></affiliation></author><author><name sortKey="Wendland, Jens R" sort="Wendland, Jens R" uniqKey="Wendland J" first="Jens R" last="Wendland">Jens R. Wendland</name></author><author><name sortKey="Rubenstein, Liza M" sort="Rubenstein, Liza M" uniqKey="Rubenstein L" first="Liza M" last="Rubenstein">Liza M. Rubenstein</name></author><author><name sortKey="Timpano, Kiara R" sort="Timpano, Kiara R" uniqKey="Timpano K" first="Kiara R" last="Timpano">Kiara R. Timpano</name></author><author><name sortKey="Heiman, Gary A" sort="Heiman, Gary A" uniqKey="Heiman G" first="Gary A" last="Heiman">Gary A. Heiman</name></author><author><name sortKey="Tischfield, Jay A" sort="Tischfield, Jay A" uniqKey="Tischfield J" first="Jay A" last="Tischfield">Jay A. Tischfield</name></author><author><name sortKey="King, Robert A" sort="King, Robert A" uniqKey="King R" first="Robert A" last="King">Robert A. King</name></author><author><name sortKey="Andrews, Anne M" sort="Andrews, Anne M" uniqKey="Andrews A" first="Anne M" last="Andrews">Anne M. Andrews</name></author><author><name sortKey="Ramamoorthy, Samanda" sort="Ramamoorthy, Samanda" uniqKey="Ramamoorthy S" first="Samanda" last="Ramamoorthy">Samanda Ramamoorthy</name></author><author><name sortKey="Mcmahon, Francis J" sort="Mcmahon, Francis J" uniqKey="Mcmahon F" first="Francis J" last="Mcmahon">Francis J. Mcmahon</name></author><author><name sortKey="Murphy, Dennis L" sort="Murphy, Dennis L" uniqKey="Murphy D" first="Dennis L" last="Murphy">Dennis L. Murphy</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Female</term><term>Gene Frequency</term><term>Genetic Association Studies</term><term>Genetic Predisposition to Disease (genetics)</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Obsessive-Compulsive Disorder (genetics)</term><term>Polymorphism, Single Nucleotide (genetics)</term><term>Psychiatric Status Rating Scales</term><term>Serotonin Plasma Membrane Transport Proteins (genetics)</term><term>Tourette Syndrome (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Serotonin Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Genetic Predisposition to Disease</term><term>Obsessive-Compulsive Disorder</term><term>Polymorphism, Single Nucleotide</term><term>Tourette Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Female</term><term>Gene Frequency</term><term>Genetic Association Studies</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Psychiatric Status Rating Scales</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To evaluate the hypothesis that functionally over-expressing alleles of the serotonin transporter (SERT) gene (solute carrier family 6, member 4, SLC6A4) are present in Tourette's disorder (TD), just as we previously observed in obsessive compulsive disorder (OCD), we evaluated TD probands (N = 151) and controls (N = 858). We genotyped the refined SERT-linked polymorphic region 5-HTTLPR/rs25531 and the associated rs25532 variant in the SLC6A4 promoter plus the rare coding variant SERT isoleucine-to-valine at position 425 (I425V). The higher expressing 5-HTTLPR/rs25531 LA allele was more prevalent in TD probands than in controls (χ(2) = 5.75; P = 0.017; odds ratio [OR], 1.35); and, in a secondary analysis, surprisingly, it was significantly more frequent in probands who had TD alone than in those who had TD plus OCD (Fisher's exact test; P = 0.0006; OR, 2.29). Likewise, the higher expressing LAC haplotype (5-HTTLPR/rs25531/rs25532) was more frequent in TD probands than in controls (P = 0.024; OR, 1.33) and also in the TD alone group versus the TD plus OCD group (P = 0.0013; OR, 2.14). Furthermore, the rare gain-of-function SERT I425V variant was observed in 3 male siblings with TD and/or OCD and in their father. Thus, the cumulative count of SERT I425V becomes 1.57% in OCD/TD spectrum conditions versus 0.15% in controls, with a recalculated, family-adjusted significance of χ(2) = 15.03 (P < 0.0001; OR, 9.0; total worldwide genotyped, 2914). This report provides a unique combination of common and rare variants in one gene in TD, all of which are associated with SERT gain of function. Thus, altered SERT activity represents a potential contributor to serotonergic abnormalities in TD. The present results call for replication in a similarly intensively evaluated sample. © 2013 Movement Disorder Society.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23630162</PMID><DateCreated><Year>2013</Year><Month>09</Month><Day>04</Day></DateCreated><DateCompleted><Year>2014</Year><Month>04</Month><Day>02</Day></DateCompleted><DateRevised><Year>2015</Year><Month>04</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>9</Issue><PubDate><Year>2013</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Common and rare alleles of the serotonin transporter gene, SLC6A4, associated with Tourette's disorder.</ArticleTitle><Pagination><MedlinePgn>1263-70</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25460</ELocationID><Abstract><AbstractText>To evaluate the hypothesis that functionally over-expressing alleles of the serotonin transporter (SERT) gene (solute carrier family 6, member 4, SLC6A4) are present in Tourette's disorder (TD), just as we previously observed in obsessive compulsive disorder (OCD), we evaluated TD probands (N = 151) and controls (N = 858). We genotyped the refined SERT-linked polymorphic region 5-HTTLPR/rs25531 and the associated rs25532 variant in the SLC6A4 promoter plus the rare coding variant SERT isoleucine-to-valine at position 425 (I425V). The higher expressing 5-HTTLPR/rs25531 LA allele was more prevalent in TD probands than in controls (χ(2) = 5.75; P = 0.017; odds ratio [OR], 1.35); and, in a secondary analysis, surprisingly, it was significantly more frequent in probands who had TD alone than in those who had TD plus OCD (Fisher's exact test; P = 0.0006; OR, 2.29). Likewise, the higher expressing LAC haplotype (5-HTTLPR/rs25531/rs25532) was more frequent in TD probands than in controls (P = 0.024; OR, 1.33) and also in the TD alone group versus the TD plus OCD group (P = 0.0013; OR, 2.14). Furthermore, the rare gain-of-function SERT I425V variant was observed in 3 male siblings with TD and/or OCD and in their father. Thus, the cumulative count of SERT I425V becomes 1.57% in OCD/TD spectrum conditions versus 0.15% in controls, with a recalculated, family-adjusted significance of χ(2) = 15.03 (P < 0.0001; OR, 9.0; total worldwide genotyped, 2914). This report provides a unique combination of common and rare variants in one gene in TD, all of which are associated with SERT gain of function. Thus, altered SERT activity represents a potential contributor to serotonergic abnormalities in TD. The present results call for replication in a similarly intensively evaluated sample. © 2013 Movement Disorder Society.</AbstractText><CopyrightInformation>Copyright © 2013 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moya</LastName><ForeName>Pablo R</ForeName><Initials>PR</Initials><AffiliationInfo><Affiliation>National Institute of Mental Health-Intramural Research Program, Bethesda, MD, USA. moyap@mail.nih.gov</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wendland</LastName><ForeName>Jens R</ForeName><Initials>JR</Initials></Author><Author ValidYN="Y"><LastName>Rubenstein</LastName><ForeName>Liza M</ForeName><Initials>LM</Initials></Author><Author ValidYN="Y"><LastName>Timpano</LastName><ForeName>Kiara R</ForeName><Initials>KR</Initials></Author><Author ValidYN="Y"><LastName>Heiman</LastName><ForeName>Gary A</ForeName><Initials>GA</Initials></Author><Author ValidYN="Y"><LastName>Tischfield</LastName><ForeName>Jay A</ForeName><Initials>JA</Initials></Author><Author ValidYN="Y"><LastName>King</LastName><ForeName>Robert A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Andrews</LastName><ForeName>Anne M</ForeName><Initials>AM</Initials></Author><Author ValidYN="Y"><LastName>Ramamoorthy</LastName><ForeName>Samanda</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>McMahon</LastName><ForeName>Francis J</ForeName><Initials>FJ</Initials></Author><Author ValidYN="Y"><LastName>Murphy</LastName><ForeName>Dennis L</ForeName><Initials>DL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 MH064756</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH092293</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-MH064756</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-MH092293</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U24 MH068457</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>Z01 MH000336-28</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>Z99 MH999999</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>ZIA MH000336-30</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>04</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493230">SLC6A4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050486">Serotonin Plasma Membrane Transport Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Cell Mol Neurobiol. 2006 Jul-Aug;26(4-6):755-80</RefSource><PMID Version="1">17029036</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2007 Jan 17;27(3):684-91</RefSource><PMID 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