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MAOA, DBH, and SLC6A4 variants in CHARGE: a case–control study of autism spectrum disorders / Flora TASSONE in Autism Research, 4-4 (August 2011)
[article]
Titre : MAOA, DBH, and SLC6A4 variants in CHARGE: a case–control study of autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : Flora TASSONE, Auteur ; Lihong QI, Auteur ; Wenting ZHANG, Auteur ; David J. HANSEN, Auteur ; Isaac N. PESSAH, Auteur ; Irva HERTZ-PICCIOTTO, Auteur Année de publication : 2011 Article en page(s) : p.250-261 Langues : Anglais (eng) Mots-clés : ASD polymorphisms SLC6A4 MAOA DBH Index. décimale : PER Périodiques Résumé : Genetic factors are established to contribute to the development of autism. We examined three loci, serotonin transporter (SLC6A4), dopamine β-hydroxylase (DBH), and the variable number of tandem repeat promoter of the monoamine oxidase A (MAOA) for association with autism in participants from the Childhood Autism Risks from Genetics and the Environment (CHARGE ) Study, the first large-scale population-based case–control investigation of both environmental and genetic contributions to autism risk. Among male children enrolled in the CHARGE study we tested associations between each of the three polymorphisms and autism (AU) (n = 119), or a combined group of autism and other autism spectrum disorders (AU+ASD, which includes an additional n = 53) as compared with typically developing controls (TD, n = 137). The case–control association analysis showed neither SLC6A4 nor DBH to be statistically significantly associated with AU or ASD. However, the male children carrying 4 tandem repeats in the promoter region of the MAOA gene showed a two-fold higher risk of AU (or AU+ASD) than those carrying allele 3, adjusted for confounders (OR = 2.02, 95% CI = 1.12, 3.65, P = 0.02 for AU vs. TD, and OR = 2.05, 95% CI = 1.19, 3.53, P = 0.01 for ASD vs. TD). In addition, children of mothers homozygous for the 4 tandem repeat allele showed at least a three-fold higher risk of AU (or AU+ASD) than those with mothers homozygous for allele 3 (OR = 3.07, 95% CI = 1.19, 7.91, P = 0.02 for AU vs. TD, and OR = 3.26, 95% CI = 1.35, 7.89, P = 0.009 for AU+ASD vs. TD). These results suggest a potential role of the functional MAOA promoter alleles in the male child, the mother, or both in ASD. En ligne : http://dx.doi.org/10.1002/aur.196 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=141
in Autism Research > 4-4 (August 2011) . - p.250-261[article] MAOA, DBH, and SLC6A4 variants in CHARGE: a case–control study of autism spectrum disorders [Texte imprimé et/ou numérique] / Flora TASSONE, Auteur ; Lihong QI, Auteur ; Wenting ZHANG, Auteur ; David J. HANSEN, Auteur ; Isaac N. PESSAH, Auteur ; Irva HERTZ-PICCIOTTO, Auteur . - 2011 . - p.250-261.
Langues : Anglais (eng)
in Autism Research > 4-4 (August 2011) . - p.250-261
Mots-clés : ASD polymorphisms SLC6A4 MAOA DBH Index. décimale : PER Périodiques Résumé : Genetic factors are established to contribute to the development of autism. We examined three loci, serotonin transporter (SLC6A4), dopamine β-hydroxylase (DBH), and the variable number of tandem repeat promoter of the monoamine oxidase A (MAOA) for association with autism in participants from the Childhood Autism Risks from Genetics and the Environment (CHARGE ) Study, the first large-scale population-based case–control investigation of both environmental and genetic contributions to autism risk. Among male children enrolled in the CHARGE study we tested associations between each of the three polymorphisms and autism (AU) (n = 119), or a combined group of autism and other autism spectrum disorders (AU+ASD, which includes an additional n = 53) as compared with typically developing controls (TD, n = 137). The case–control association analysis showed neither SLC6A4 nor DBH to be statistically significantly associated with AU or ASD. However, the male children carrying 4 tandem repeats in the promoter region of the MAOA gene showed a two-fold higher risk of AU (or AU+ASD) than those carrying allele 3, adjusted for confounders (OR = 2.02, 95% CI = 1.12, 3.65, P = 0.02 for AU vs. TD, and OR = 2.05, 95% CI = 1.19, 3.53, P = 0.01 for ASD vs. TD). In addition, children of mothers homozygous for the 4 tandem repeat allele showed at least a three-fold higher risk of AU (or AU+ASD) than those with mothers homozygous for allele 3 (OR = 3.07, 95% CI = 1.19, 7.91, P = 0.02 for AU vs. TD, and OR = 3.26, 95% CI = 1.35, 7.89, P = 0.009 for AU+ASD vs. TD). These results suggest a potential role of the functional MAOA promoter alleles in the male child, the mother, or both in ASD. En ligne : http://dx.doi.org/10.1002/aur.196 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=141 Gene–environment interaction in externalizing problems among adolescents: evidence from the Pelotas 1993 Birth Cohort Study / Christian KIELING in Journal of Child Psychology and Psychiatry, 54-3 (March 2013)
[article]
Titre : Gene–environment interaction in externalizing problems among adolescents: evidence from the Pelotas 1993 Birth Cohort Study Type de document : Texte imprimé et/ou numérique Auteurs : Christian KIELING, Auteur ; Mara H. HUTZ, Auteur ; Júlia P. GENRO, Auteur ; Guilherme V. POLANCZYK, Auteur ; Luciana ANSELMI, Auteur ; Suzi CAMEY, Auteur ; Pedro C. HALLAL, Auteur ; Fernando C. BARROS, Auteur ; Cesar G. VICTORA, Auteur ; Ana Maria B. MENEZES, Auteur ; Luis Augusto ROHDE, Auteur Article en page(s) : p.298-304 Mots-clés : Gene–environment interaction DAT1 maternal smoking MAOA childhood maltreatment externalizing Index. décimale : PER Périodiques Résumé : Background: The study of gene–environment interactions (G × E) is one of the most promising strategies to uncover the origins of mental disorders. Replication of initial findings, however, is essential because there is a strong possibility of publication bias in the literature. In addition, there is a scarcity of research on the topic originated from low- and middle-income countries (LMIC). The aim of this study was to replicate G × E hypotheses for externalizing problems among adolescents in a middle-income country. Methods: As part of the Pelotas 1993 Birth Cohort Study, 5,249 children were enrolled at birth and followed up to the age of 15 years, with an 85.7% retention rate. We sought an interaction between the homozygosity of the 10-repeat allele at the dopamine transporter (DAT1) gene and prenatal maternal smoking in the development of hyperactivity problems during adolescence assessed by the Strengths and Difficulties Questionnaire. We also tested for an interaction between the uVNTR polymorphism at the monoamine oxidase A (MAOA) and the experience of childhood maltreatment in the occurrence of conduct problems among adolescent boys. Results: Although there was a clear association between prenatal maternal smoking and hyperactivity scores in adolescence (p 0.001), no main genetic or interaction effects for the DAT1 gene were detected. Similarly, childhood maltreatment showed to be associated with conduct problems among boys (p 0.001), with no observable main genetic or interaction effects for the MAOA gene. Conclusions: In the largest mental health G × E study performed in a LMIC to date, we did not replicate previous positive findings from the literature. Despite the presence of main environmental effects, there was no evidence of effect modification by genotype status. Additional replication efforts to measure G × E are needed to better understand the origins of mental health and illness, especially in LMIC. En ligne : http://dx.doi.org/10.1111/jcpp.12022 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=191
in Journal of Child Psychology and Psychiatry > 54-3 (March 2013) . - p.298-304[article] Gene–environment interaction in externalizing problems among adolescents: evidence from the Pelotas 1993 Birth Cohort Study [Texte imprimé et/ou numérique] / Christian KIELING, Auteur ; Mara H. HUTZ, Auteur ; Júlia P. GENRO, Auteur ; Guilherme V. POLANCZYK, Auteur ; Luciana ANSELMI, Auteur ; Suzi CAMEY, Auteur ; Pedro C. HALLAL, Auteur ; Fernando C. BARROS, Auteur ; Cesar G. VICTORA, Auteur ; Ana Maria B. MENEZES, Auteur ; Luis Augusto ROHDE, Auteur . - p.298-304.
in Journal of Child Psychology and Psychiatry > 54-3 (March 2013) . - p.298-304
Mots-clés : Gene–environment interaction DAT1 maternal smoking MAOA childhood maltreatment externalizing Index. décimale : PER Périodiques Résumé : Background: The study of gene–environment interactions (G × E) is one of the most promising strategies to uncover the origins of mental disorders. Replication of initial findings, however, is essential because there is a strong possibility of publication bias in the literature. In addition, there is a scarcity of research on the topic originated from low- and middle-income countries (LMIC). The aim of this study was to replicate G × E hypotheses for externalizing problems among adolescents in a middle-income country. Methods: As part of the Pelotas 1993 Birth Cohort Study, 5,249 children were enrolled at birth and followed up to the age of 15 years, with an 85.7% retention rate. We sought an interaction between the homozygosity of the 10-repeat allele at the dopamine transporter (DAT1) gene and prenatal maternal smoking in the development of hyperactivity problems during adolescence assessed by the Strengths and Difficulties Questionnaire. We also tested for an interaction between the uVNTR polymorphism at the monoamine oxidase A (MAOA) and the experience of childhood maltreatment in the occurrence of conduct problems among adolescent boys. Results: Although there was a clear association between prenatal maternal smoking and hyperactivity scores in adolescence (p 0.001), no main genetic or interaction effects for the DAT1 gene were detected. Similarly, childhood maltreatment showed to be associated with conduct problems among boys (p 0.001), with no observable main genetic or interaction effects for the MAOA gene. Conclusions: In the largest mental health G × E study performed in a LMIC to date, we did not replicate previous positive findings from the literature. Despite the presence of main environmental effects, there was no evidence of effect modification by genotype status. Additional replication efforts to measure G × E are needed to better understand the origins of mental health and illness, especially in LMIC. En ligne : http://dx.doi.org/10.1111/jcpp.12022 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=191