Glial cell line-derived neurotrophic factor receptor alpha 2 (GFRA2) gene is associated with tardive dyskinesia
Identifieur interne : 001D10 ( Main/Exploration ); précédent : 001D09; suivant : 001D11Glial cell line-derived neurotrophic factor receptor alpha 2 (GFRA2) gene is associated with tardive dyskinesia
Auteurs : Renan P. Souza [Canada] ; Vincenzo De Luca [Canada] ; Gary Remington [Canada] ; Jeffrey A. Lieberman [États-Unis] ; Herbert Y. Meltzer [États-Unis] ; James L. Kennedy [Canada] ; Albert H. C. Wong [Canada]Source :
- Psychopharmacologia [ 0033-3158 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
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Abstract
Introduction Tardive dyskinesia (TD) has a pharmacogenetic component in which the interaction of antipsychotic exposure with individual genetic variation mediates risk. The glial cell line-derived neurotrophic factor (GDNF) signalling pathway has been associated with neuroprotective effects in central dopaminergic neurons and spinal motor neurons. Clinical trials have also investigated whether GDNF may ameliorate Parkinson's disease symptoms. Methods We tested whether variants in the GDNF receptor alpha 2 (GFRA2) gene could play a role in TD susceptibility evaluating 16 variants in 172 Caucasian schizophrenia subjects. Results We observed one significant allelic association (rs4739285, permuted p=0.042) and two genotypic associations: rs4739285 under additive inheritance model and rs4739217 under dominant inheritance model (permuted p=0.044). Moreover, carriers of the major alleles for both rs6587002 and rs4739217 presented significantly higher risk for TD (OR=2.04, permuted p=0.014), while subjects with the minor allele for rs4739217 and the major allele for rs6988470 were less likely to have TD (OR=0.21, permuted p=0.0007). Discussion Haplotype results indicate that the minor allele of the rs4739217 is a risk factor for TD (permuted allelic p=0.074). Age was also a risk factor for TD in our sample (p=0.0001). Taken together, our findings suggest that GFRA2 genetic variants and age may play a role in TD susceptibility, but further work is required to confirm these findings.
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Souza</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurogenetics Section, Neuroscience Department, Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, Ontario</wicri:noRegion></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="De Luca, Vincenzo" sort="De Luca, Vincenzo" uniqKey="De Luca V" first="Vincenzo" last="De Luca">Vincenzo De Luca</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurogenetics Section, Neuroscience Department, Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, Ontario</wicri:noRegion></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Remington, Gary" sort="Remington, Gary" uniqKey="Remington G" first="Gary" last="Remington">Gary Remington</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurogenetics Section, Neuroscience Department, Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, Ontario</wicri:noRegion></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Lieberman, Jeffrey A" sort="Lieberman, Jeffrey A" uniqKey="Lieberman J" first="Jeffrey A." last="Lieberman">Jeffrey A. Lieberman</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>New York State Psychiatric Institute, Columbia University Medical Centre</s1><s2>New York City, NY</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>New York City, NY</wicri:noRegion></affiliation></author><author><name sortKey="Meltzer, Herbert Y" sort="Meltzer, Herbert Y" uniqKey="Meltzer H" first="Herbert Y." last="Meltzer">Herbert Y. Meltzer</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Psychiatric Hospital, Vanderbilt University</s1><s2>Nashville, TN</s2><s3>USA</s3><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Nashville, TN</wicri:noRegion></affiliation></author><author><name sortKey="Kennedy, James L" sort="Kennedy, James L" uniqKey="Kennedy J" first="James L." last="Kennedy">James L. Kennedy</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neurogenetics Section, Neuroscience Department, Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, Ontario</wicri:noRegion></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Wong, Albert H C" sort="Wong, Albert H C" uniqKey="Wong A" first="Albert H. C." last="Wong">Albert H. C. Wong</name><affiliation wicri:level="4"><inist:fA14 i1="05"><s1>Department of Pharmacology, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>7 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Neurobiology of Schizophrenia Section, Neuroscience Department, Centre for Addiction and Mental Health</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>7 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, Ontario</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Psychopharmacologia</title><title level="j" type="abbreviated">Psychopharmacologia</title><idno type="ISSN">0033-3158</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Psychopharmacologia</title><title level="j" type="abbreviated">Psychopharmacologia</title><idno type="ISSN">0033-3158</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Biological receptor</term><term>Dyskinesia</term><term>Gene</term><term>Glial cell line derived neurotrophic factor</term><term>Late</term><term>Motility disorder</term><term>Motor control</term><term>Motor system disorder</term><term>Parkinson disease</term><term>Pharmacogenetics</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Facteur GDNF</term><term>Récepteur biologique</term><term>Gène</term><term>Dyskinésie</term><term>Tardif</term><term>Trouble motricité</term><term>Trouble moteur</term><term>Maladie de Parkinson</term><term>Pharmacogénétique</term><term>Contrôle moteur</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Introduction Tardive dyskinesia (TD) has a pharmacogenetic component in which the interaction of antipsychotic exposure with individual genetic variation mediates risk. The glial cell line-derived neurotrophic factor (GDNF) signalling pathway has been associated with neuroprotective effects in central dopaminergic neurons and spinal motor neurons. Clinical trials have also investigated whether GDNF may ameliorate Parkinson's disease symptoms. Methods We tested whether variants in the GDNF receptor alpha 2 (GFRA2) gene could play a role in TD susceptibility evaluating 16 variants in 172 Caucasian schizophrenia subjects. Results We observed one significant allelic association (rs4739285, permuted p=0.042) and two genotypic associations: rs4739285 under additive inheritance model and rs4739217 under dominant inheritance model (permuted p=0.044). Moreover, carriers of the major alleles for both rs6587002 and rs4739217 presented significantly higher risk for TD (OR=2.04, permuted p=0.014), while subjects with the minor allele for rs4739217 and the major allele for rs6988470 were less likely to have TD (OR=0.21, permuted p=0.0007). Discussion Haplotype results indicate that the minor allele of the rs4739217 is a risk factor for TD (permuted allelic p=0.074). Age was also a risk factor for TD in our sample (p=0.0001). Taken together, our findings suggest that GFRA2 genetic variants and age may play a role in TD susceptibility, but further work is required to confirm these findings.</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="Canada"><noRegion><name sortKey="Souza, Renan P" sort="Souza, Renan P" uniqKey="Souza R" first="Renan P." last="Souza">Renan P. Souza</name></noRegion><name sortKey="De Luca, Vincenzo" sort="De Luca, Vincenzo" uniqKey="De Luca V" first="Vincenzo" last="De Luca">Vincenzo De Luca</name><name sortKey="De Luca, Vincenzo" sort="De Luca, Vincenzo" uniqKey="De Luca V" first="Vincenzo" last="De Luca">Vincenzo De Luca</name><name sortKey="Kennedy, James L" sort="Kennedy, James L" uniqKey="Kennedy J" first="James L." last="Kennedy">James L. Kennedy</name><name sortKey="Kennedy, James L" sort="Kennedy, James L" uniqKey="Kennedy J" first="James L." last="Kennedy">James L. Kennedy</name><name sortKey="Remington, Gary" sort="Remington, Gary" uniqKey="Remington G" first="Gary" last="Remington">Gary Remington</name><name sortKey="Remington, Gary" sort="Remington, Gary" uniqKey="Remington G" first="Gary" last="Remington">Gary Remington</name><name sortKey="Souza, Renan P" sort="Souza, Renan P" uniqKey="Souza R" first="Renan P." last="Souza">Renan P. Souza</name><name sortKey="Wong, Albert H C" sort="Wong, Albert H C" uniqKey="Wong A" first="Albert H. C." last="Wong">Albert H. C. Wong</name><name sortKey="Wong, Albert H C" sort="Wong, Albert H C" uniqKey="Wong A" first="Albert H. C." last="Wong">Albert H. C. Wong</name></country><country name="États-Unis"><noRegion><name sortKey="Lieberman, Jeffrey A" sort="Lieberman, Jeffrey A" uniqKey="Lieberman J" first="Jeffrey A." last="Lieberman">Jeffrey A. Lieberman</name></noRegion><name sortKey="Meltzer, Herbert Y" sort="Meltzer, Herbert Y" uniqKey="Meltzer H" first="Herbert Y." last="Meltzer">Herbert Y. Meltzer</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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