Cholinergic nicotinic receptor genes implicated in a nicotine dependence association study targeting 348 candidate genes with 3713 SNPs
Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström t...
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| Published in | Human molecular genetics Vol. 16; no. 1; pp. 36 - 49 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Oxford University Press
01.01.2007
Oxford Publishing Limited (England) |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the β3 nicotinic receptor subunit gene (P = 9.4 × 10−5). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the α5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 × 10−4). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies. |
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| AbstractList | Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the β3 nicotinic receptor subunit gene (P = 9.4 × 10-5). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the α5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 × 10-4). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies. Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the β3 nicotinic receptor subunit gene (P = 9.4 × 10−5). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the α5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 × 10−4). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies. Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the beta3 nicotinic receptor subunit gene (P = 9.4 x 10(-5)). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the alpha5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 x 10(-4)). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies. Nicotine dependence is one of the world’s leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3 , the β 3 nicotinic receptor subunit gene ( P = 9.4 × 10 −5 ). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the α 5 nicotinic receptor subunit gene CHRNA5 ( P = 6.4 × 10 −4 ). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4 . This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies. Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the beta3 nicotinic receptor subunit gene (P = 9.4 x 10(-5)). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the alpha5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 x 10(-4)). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies.Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the beta3 nicotinic receptor subunit gene (P = 9.4 x 10(-5)). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the alpha5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 x 10(-4)). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies. Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerstroem test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the {szligbeta}3 nicotinic receptor subunit gene (P = 9.4 x 10 super(-5)). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the alpha 5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 x 10 super(-4)). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies. |
| Author | Fugman, Douglas Goate, Alison M. Saccone, Scott F. Saccone, Nancy L. Madden, Pamela A.F. Fox, Louis Hatsukami, Dorothy Rutter, Joni Bertelsen, Sarah Hinrichs, Anthony L. Rice, John P. Konvicka, Karel Wang, Jen C. Swan, Gary E. Breslau, Naomi Johnson, Eric O. Montgomery, Grant W. Chase, Gary A. Pomerleau, Ovide Ballinger, Dennis G. Martin, Nicholas G. Bierut, Laura Jean |
| AuthorAffiliation | 2 Department of Genetics, Box 8134, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA 3 Department of Health Evaluation Sciences, Penn State College of Medicine, Hershey, PA 17033, USA 4 Perlegen Sciences, Mountain View, CA 94043, USA 7 Department of Psychiatry, University of Minnesota, Minneapolis, MN 55454, USA 12 Queensland Institute of Medical Research, Queensland 4029, Australia 9 Center for Health Sciences, SRI International, Menlo Park, CA 94025, USA 10 National Institute on Drug Abuse, Bethesda, MD 20892, USA 6 Research Triangle Institute International, Research Triangle Park, NC 27709, USA 11 Rutgers University Cell and DNA Repository, Rutgers University, Piscataway, NJ 08854, USA 1 Department of Psychiatry, Box 8134, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA 5 Department of Epidemiology, Michigan State University, East Lansing, MI 48824, USA 8 Department of Psychiatry, University of Michigan, Ann A |
| AuthorAffiliation_xml | – name: 5 Department of Epidemiology, Michigan State University, East Lansing, MI 48824, USA – name: 4 Perlegen Sciences, Mountain View, CA 94043, USA – name: 10 National Institute on Drug Abuse, Bethesda, MD 20892, USA – name: 7 Department of Psychiatry, University of Minnesota, Minneapolis, MN 55454, USA – name: 1 Department of Psychiatry, Box 8134, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA – name: 6 Research Triangle Institute International, Research Triangle Park, NC 27709, USA – name: 2 Department of Genetics, Box 8134, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA – name: 3 Department of Health Evaluation Sciences, Penn State College of Medicine, Hershey, PA 17033, USA – name: 9 Center for Health Sciences, SRI International, Menlo Park, CA 94025, USA – name: 12 Queensland Institute of Medical Research, Queensland 4029, Australia – name: 8 Department of Psychiatry, University of Michigan, Ann Arbor, MI 48109, USA – name: 11 Rutgers University Cell and DNA Repository, Rutgers University, Piscataway, NJ 08854, USA |
| Author_xml | – sequence: 1 givenname: Scott F. surname: Saccone fullname: Saccone, Scott F. email: saccones@msnotes.wustl.edu organization: 1 Department of Psychiatry and – sequence: 2 givenname: Anthony L. surname: Hinrichs fullname: Hinrichs, Anthony L. organization: 1 Department of Psychiatry and – sequence: 3 givenname: Nancy L. surname: Saccone fullname: Saccone, Nancy L. email: saccones@msnotes.wustl.edu organization: 1 Department of Psychiatry and – sequence: 4 givenname: Gary A. surname: Chase fullname: Chase, Gary A. organization: 3 Department of Health Evaluation Sciences, Penn State College of Medicine, Hershey, PA 17033, USA – sequence: 5 givenname: Karel surname: Konvicka fullname: Konvicka, Karel organization: 4 Perlegen Sciences, Mountain View, CA 94043, USA – sequence: 6 givenname: Pamela A.F. surname: Madden fullname: Madden, Pamela A.F. organization: 1 Department of Psychiatry and – sequence: 7 givenname: Naomi surname: Breslau fullname: Breslau, Naomi organization: 5 Department of Epidemiology, Michigan State University, East Lansing, MI 48824, USA – sequence: 8 givenname: Eric O. surname: Johnson fullname: Johnson, Eric O. organization: 6 Research Triangle Institute International, Research Triangle Park, NC 27709, USA – sequence: 9 givenname: Dorothy surname: Hatsukami fullname: Hatsukami, Dorothy organization: 7 Department of Psychiatry, University of Minnesota, Minneapolis, MN 55454, USA – sequence: 10 givenname: Ovide surname: Pomerleau fullname: Pomerleau, Ovide organization: 8 Department of Psychiatry, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 11 givenname: Gary E. surname: Swan fullname: Swan, Gary E. organization: 9 Center for Health Sciences, SRI International, Menlo Park, CA 94025, USA – sequence: 12 givenname: Alison M. surname: Goate fullname: Goate, Alison M. organization: 1 Department of Psychiatry and – sequence: 13 givenname: Joni surname: Rutter fullname: Rutter, Joni organization: 10 National Institute on Drug Abuse, Bethesda, MD 20892, USA – sequence: 14 givenname: Sarah surname: Bertelsen fullname: Bertelsen, Sarah organization: 1 Department of Psychiatry and – sequence: 15 givenname: Louis surname: Fox fullname: Fox, Louis organization: 1 Department of Psychiatry and – sequence: 16 givenname: Douglas surname: Fugman fullname: Fugman, Douglas organization: 11 Rutgers University Cell and DNA Repository, Rutgers University, Piscataway, NJ 08854, USA and – sequence: 17 givenname: Nicholas G. surname: Martin fullname: Martin, Nicholas G. organization: 12 Queensland Institute of Medical Research, Queensland 4029, Australia – sequence: 18 givenname: Grant W. surname: Montgomery fullname: Montgomery, Grant W. organization: 12 Queensland Institute of Medical Research, Queensland 4029, Australia – sequence: 19 givenname: Jen C. surname: Wang fullname: Wang, Jen C. organization: 1 Department of Psychiatry and – sequence: 20 givenname: Dennis G. surname: Ballinger fullname: Ballinger, Dennis G. organization: 4 Perlegen Sciences, Mountain View, CA 94043, USA – sequence: 21 givenname: John P. surname: Rice fullname: Rice, John P. organization: 1 Department of Psychiatry and – sequence: 22 givenname: Laura Jean surname: Bierut fullname: Bierut, Laura Jean organization: 1 Department of Psychiatry and |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18501652$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17135278$$D View this record in MEDLINE/PubMed |
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| Keywords | Cholinergic receptor Association Targeting Dependence Genetics Candidate gene Single nucleotide polymorphism Nicotinic receptor Nicotine |
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| Snippet | Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we... Nicotine dependence is one of the world’s leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we... |
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| SubjectTerms | Adult Aged Aged, 80 and over Biological and medical sciences Case-Control Studies Chromosomes, Human, Pair 8 Cluster Analysis Female Fundamental and applied biological sciences. Psychology Genetic Markers - genetics Genetic Variation Genetics of eukaryotes. Biological and molecular evolution Genotype Humans Male Middle Aged Molecular and cellular biology Polymorphism, Single Nucleotide Receptors, Nicotinic - genetics Tobacco Use Disorder - genetics |
| Title | Cholinergic nicotinic receptor genes implicated in a nicotine dependence association study targeting 348 candidate genes with 3713 SNPs |
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