Evidence for association of the GLI2 gene with tardive dyskinesia in patients with chronic schizophrenia.
Identifieur interne : 001901 ( PubMed/Checkpoint ); précédent : 001900; suivant : 001902Evidence for association of the GLI2 gene with tardive dyskinesia in patients with chronic schizophrenia.
Auteurs : Lior Greenbaum [Israël] ; Anna Alkelai ; Amihai Rigbi ; Yoav Kohn ; Bernard LererSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Adult, Antipsychotic Agents (adverse effects), Cross-Sectional Studies, Dyskinesia, Drug-Induced (complications), Dyskinesia, Drug-Induced (genetics), Female, Genetic Association Studies, Genetic Predisposition to Disease, Genotype, Humans, Kruppel-Like Transcription Factors (genetics), Logistic Models, Male, Middle Aged, Nuclear Proteins (genetics), Polymorphism, Single Nucleotide, Retrospective Studies, Schizophrenia (complications), Schizophrenia (drug therapy), Schizophrenia (genetics).
- MESH :
- chemical , adverse effects : Antipsychotic Agents.
- complications : Dyskinesia, Drug-Induced, Schizophrenia.
- drug therapy : Schizophrenia.
- genetics : Dyskinesia, Drug-Induced, Kruppel-Like Transcription Factors, Nuclear Proteins, Schizophrenia.
- Adult, Cross-Sectional Studies, Female, Genetic Association Studies, Genetic Predisposition to Disease, Genotype, Humans, Logistic Models, Male, Middle Aged, Polymorphism, Single Nucleotide, Retrospective Studies.
Abstract
Tardive dyskinesia (TD) occurs in approximately 20% of patients exposed to long-term antipsychotic treatment and may be influenced by genetic predisposition, in addition to clinical risk factors. In this study, we implemented a two-step approach to identify susceptibility genes for TD. First, we performed a secondary analysis of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) genome-wide association study (GWAS) dataset to identify candidate genes for TD severity. A total of 327 schizophrenia patients treated with antipsychotics who participated in the CATIE trial were included in a TD severity GWAS (approximately 495,000 SNPs). Cases were defined as demonstrating involuntary movements of a mild degree in two or more body regions or of a moderate to severe degree in at least one body region on at least two separate evaluations, whereas controls were completely free of abnormal involuntary movement on all evaluations. Using logistic regression and controlling for population stratification and relevant clinical risk factors, none of the associated SNPs reached GWAS significance; however, several promising SNPs were identified for follow-up investigation. In the second step, we performed an association study of the top 25 SNPs in an independent sample of 170 Jewish, Israeli, schizophrenia patients (retrospective, cross-sectional design). Association of the SNP rs3943552 T allele in the GLI2 gene with TD was observed in a subsample of Ashkenazi Jewish patients (N = 96, P = 0.018; P = 6.2 × 10⁻⁵ in the CATIE sample). The GLI2 gene encodes a transcription factor that participates in the development of the dopaminergic system during embryogenesis. Taken together, our findings support a possible contribution of GLI2 to TD susceptibility.
DOI: 10.1002/mds.23377
PubMed: 20939080
Affiliations:
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last="Rigbi">Amihai Rigbi</name></author><author><name sortKey="Kohn, Yoav" sort="Kohn, Yoav" uniqKey="Kohn Y" first="Yoav" last="Kohn">Yoav Kohn</name></author><author><name sortKey="Lerer, Bernard" sort="Lerer, Bernard" uniqKey="Lerer B" first="Bernard" last="Lerer">Bernard Lerer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.23377</idno><idno type="RBID">pubmed:20939080</idno><idno type="pmid">20939080</idno><idno type="wicri:Area/PubMed/Corpus">001517</idno><idno type="wicri:Area/PubMed/Curation">001517</idno><idno type="wicri:Area/PubMed/Checkpoint">001901</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Evidence for association of the GLI2 gene with tardive dyskinesia in patients with chronic schizophrenia.</title><author><name sortKey="Greenbaum, Lior" sort="Greenbaum, Lior" uniqKey="Greenbaum L" first="Lior" last="Greenbaum">Lior 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Lerer</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="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antipsychotic Agents (adverse effects)</term><term>Cross-Sectional Studies</term><term>Dyskinesia, Drug-Induced (complications)</term><term>Dyskinesia, Drug-Induced (genetics)</term><term>Female</term><term>Genetic Association Studies</term><term>Genetic Predisposition to Disease</term><term>Genotype</term><term>Humans</term><term>Kruppel-Like Transcription Factors (genetics)</term><term>Logistic Models</term><term>Male</term><term>Middle Aged</term><term>Nuclear Proteins (genetics)</term><term>Polymorphism, Single Nucleotide</term><term>Retrospective Studies</term><term>Schizophrenia (complications)</term><term>Schizophrenia (drug therapy)</term><term>Schizophrenia (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antipsychotic Agents</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Kruppel-Like Transcription Factors</term><term>Nuclear Proteins</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Cross-Sectional Studies</term><term>Female</term><term>Genetic Association Studies</term><term>Genetic Predisposition to Disease</term><term>Genotype</term><term>Humans</term><term>Logistic Models</term><term>Male</term><term>Middle Aged</term><term>Polymorphism, Single Nucleotide</term><term>Retrospective Studies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tardive dyskinesia (TD) occurs in approximately 20% of patients exposed to long-term antipsychotic treatment and may be influenced by genetic predisposition, in addition to clinical risk factors. In this study, we implemented a two-step approach to identify susceptibility genes for TD. First, we performed a secondary analysis of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) genome-wide association study (GWAS) dataset to identify candidate genes for TD severity. A total of 327 schizophrenia patients treated with antipsychotics who participated in the CATIE trial were included in a TD severity GWAS (approximately 495,000 SNPs). Cases were defined as demonstrating involuntary movements of a mild degree in two or more body regions or of a moderate to severe degree in at least one body region on at least two separate evaluations, whereas controls were completely free of abnormal involuntary movement on all evaluations. Using logistic regression and controlling for population stratification and relevant clinical risk factors, none of the associated SNPs reached GWAS significance; however, several promising SNPs were identified for follow-up investigation. In the second step, we performed an association study of the top 25 SNPs in an independent sample of 170 Jewish, Israeli, schizophrenia patients (retrospective, cross-sectional design). Association of the SNP rs3943552 T allele in the GLI2 gene with TD was observed in a subsample of Ashkenazi Jewish patients (N = 96, P = 0.018; P = 6.2 × 10⁻⁵ in the CATIE sample). The GLI2 gene encodes a transcription factor that participates in the development of the dopaminergic system during embryogenesis. Taken together, our findings support a possible contribution of GLI2 to TD susceptibility.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20939080</PMID><DateCreated><Year>2010</Year><Month>12</Month><Day>17</Day></DateCreated><DateCompleted><Year>2011</Year><Month>04</Month><Day>08</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>16</Issue><PubDate><Year>2010</Year><Month>Dec</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Evidence for association of the GLI2 gene with tardive dyskinesia in patients with chronic schizophrenia.</ArticleTitle><Pagination><MedlinePgn>2809-17</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23377</ELocationID><Abstract><AbstractText>Tardive dyskinesia (TD) occurs in approximately 20% of patients exposed to long-term antipsychotic treatment and may be influenced by genetic predisposition, in addition to clinical risk factors. In this study, we implemented a two-step approach to identify susceptibility genes for TD. First, we performed a secondary analysis of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) genome-wide association study (GWAS) dataset to identify candidate genes for TD severity. A total of 327 schizophrenia patients treated with antipsychotics who participated in the CATIE trial were included in a TD severity GWAS (approximately 495,000 SNPs). Cases were defined as demonstrating involuntary movements of a mild degree in two or more body regions or of a moderate to severe degree in at least one body region on at least two separate evaluations, whereas controls were completely free of abnormal involuntary movement on all evaluations. Using logistic regression and controlling for population stratification and relevant clinical risk factors, none of the associated SNPs reached GWAS significance; however, several promising SNPs were identified for follow-up investigation. In the second step, we performed an association study of the top 25 SNPs in an independent sample of 170 Jewish, Israeli, schizophrenia patients (retrospective, cross-sectional design). Association of the SNP rs3943552 T allele in the GLI2 gene with TD was observed in a subsample of Ashkenazi Jewish patients (N = 96, P = 0.018; P = 6.2 × 10⁻⁵ in the CATIE sample). The GLI2 gene encodes a transcription factor that participates in the development of the dopaminergic system during embryogenesis. 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Lerer</name><name sortKey="Rigbi, Amihai" sort="Rigbi, Amihai" uniqKey="Rigbi A" first="Amihai" last="Rigbi">Amihai Rigbi</name></noCountry><country name="Israël"><noRegion><name sortKey="Greenbaum, Lior" sort="Greenbaum, Lior" uniqKey="Greenbaum L" first="Lior" last="Greenbaum">Lior Greenbaum</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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