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The serotonin transporter gene polymorphism 5-HTTLPR moderates the effects of stress on attention-deficit/hyperactivity disorder / Dennis VAN DER MEER in Journal of Child Psychology and Psychiatry, 55-12 (December 2014)
[article]
Titre : The serotonin transporter gene polymorphism 5-HTTLPR moderates the effects of stress on attention-deficit/hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : Dennis VAN DER MEER, Auteur ; Catharina A. HARTMAN, Auteur ; Jennifer RICHARDS, Auteur ; Janita B. BRALTEN, Auteur ; Barbara FRANKE, Auteur ; Jaap OOSTERLAAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Stephen V. FARAONE, Auteur ; Jan K. BUITELAAR, Auteur ; Pieter J. HOEKSTRA, Auteur Article en page(s) : p.1363-1371 Langues : Anglais (eng) Mots-clés : ADHD gene–environment interaction (GxE) stress serotonin transporter (5-HTTLPR) Index. décimale : PER Périodiques Résumé : Introduction The role of the serotonin transporter gene polymorphism 5-HTTLPR in attention-deficit/hyperactivity disorder (ADHD) is unclear. Heterogeneity of findings may be explained by gene–environment interactions (GxE), as it has been suggested that S-allele carriers are more reactive to psychosocial stress than L-allele homozygotes. This study aimed to investigate whether 5-HTTLPR genotype moderates the effects of stress on ADHD in a multisite prospective ADHD cohort study. Methods 5-HTTLPR genotype, as well as the number of stressful life events in the past 5 years and ongoing long-term difficulties, was determined in 671 adolescents and young adults with ADHD, their siblings, and healthy controls (57.4% male, average age 17.3 years). Linear mixed models, accounting for family relatedness, were applied to investigate the effects of genotype, experienced stress, and their interaction on ADHD severity at time point T2, while controlling for ADHD severity at T1 (mean follow-up time 5.9 years) and for comorbid internalizing problems at T2. Results The interaction between genotype and stress significantly predicted ADHD severity at T2 (p = .006), which was driven by the effect on hyperactivity–impulsivity (p = .004). Probing of the interaction effect made clear that S-allele carriers had a significantly more positive correlation between stress and ADHD severity than L-allele homozygotes. Conclusion The results show that the interaction between 5-HTTLPR and stress is a mechanism involved particularly in the hyperactivity/impulsivity dimension of ADHD, and that this is independent of comorbid internalizing problems. Further research into the neurobiological mechanisms underlying this interaction effect is warranted. En ligne : http://dx.doi.org/10.1111/jcpp.12240 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=243
in Journal of Child Psychology and Psychiatry > 55-12 (December 2014) . - p.1363-1371[article] The serotonin transporter gene polymorphism 5-HTTLPR moderates the effects of stress on attention-deficit/hyperactivity disorder [Texte imprimé et/ou numérique] / Dennis VAN DER MEER, Auteur ; Catharina A. HARTMAN, Auteur ; Jennifer RICHARDS, Auteur ; Janita B. BRALTEN, Auteur ; Barbara FRANKE, Auteur ; Jaap OOSTERLAAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Stephen V. FARAONE, Auteur ; Jan K. BUITELAAR, Auteur ; Pieter J. HOEKSTRA, Auteur . - p.1363-1371.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 55-12 (December 2014) . - p.1363-1371
Mots-clés : ADHD gene–environment interaction (GxE) stress serotonin transporter (5-HTTLPR) Index. décimale : PER Périodiques Résumé : Introduction The role of the serotonin transporter gene polymorphism 5-HTTLPR in attention-deficit/hyperactivity disorder (ADHD) is unclear. Heterogeneity of findings may be explained by gene–environment interactions (GxE), as it has been suggested that S-allele carriers are more reactive to psychosocial stress than L-allele homozygotes. This study aimed to investigate whether 5-HTTLPR genotype moderates the effects of stress on ADHD in a multisite prospective ADHD cohort study. Methods 5-HTTLPR genotype, as well as the number of stressful life events in the past 5 years and ongoing long-term difficulties, was determined in 671 adolescents and young adults with ADHD, their siblings, and healthy controls (57.4% male, average age 17.3 years). Linear mixed models, accounting for family relatedness, were applied to investigate the effects of genotype, experienced stress, and their interaction on ADHD severity at time point T2, while controlling for ADHD severity at T1 (mean follow-up time 5.9 years) and for comorbid internalizing problems at T2. Results The interaction between genotype and stress significantly predicted ADHD severity at T2 (p = .006), which was driven by the effect on hyperactivity–impulsivity (p = .004). Probing of the interaction effect made clear that S-allele carriers had a significantly more positive correlation between stress and ADHD severity than L-allele homozygotes. Conclusion The results show that the interaction between 5-HTTLPR and stress is a mechanism involved particularly in the hyperactivity/impulsivity dimension of ADHD, and that this is independent of comorbid internalizing problems. Further research into the neurobiological mechanisms underlying this interaction effect is warranted. En ligne : http://dx.doi.org/10.1111/jcpp.12240 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=243 Prenatal depression and 5-HTTLPR interact to predict dysregulation from 3 to 36 months – A differential susceptibility model / Vanessa BABINEAU in Journal of Child Psychology and Psychiatry, 56-1 (January 2015)
[article]
Titre : Prenatal depression and 5-HTTLPR interact to predict dysregulation from 3 to 36 months – A differential susceptibility model Type de document : Texte imprimé et/ou numérique Auteurs : Vanessa BABINEAU, Auteur ; Cathryn Gordon GREEN, Auteur ; Alexis JOLICOEUR-MARTINEAU, Auteur ; Andrée-Anne BOUVETTE-TURCOT, Auteur ; Klaus MINDE, Auteur ; Roberto SASSI, Auteur ; Martin ST-ANDRÉ, Auteur ; Normand J. CARREY, Auteur ; Leslie ATKINSON, Auteur ; James L. KENNEDY, Auteur ; John LYDON, Auteur ; Meir STEINER, Auteur ; Helene GAUDREAU, Auteur ; Robert LEVITAN, Auteur ; Michael MEANEY, Auteur ; Ashley WAZANA, Auteur ; THE MAVAN PROJECT,, Auteur Article en page(s) : p.21-29 Langues : Anglais (eng) Mots-clés : Child development emotional dysregulation gene–environment interaction (GxE) longitudinal studies maternal depression Prenatal Index. décimale : PER Périodiques Résumé : Background Childhood dysregulation, which reflects deficits in the capacity to regulate or control one's thoughts, emotions and behaviours, is associated with psychopathology throughout childhood and into adulthood. Exposures to adversity during the prenatal period, including prenatal depression, can influence the development of dysregulation, and a number of candidate genes have been suggested as moderators of prenatal exposure, including polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR). We examined whether prenatal depression and child 5-HTTLPR interact to predict childhood dysregulation. Method Sample of N = 213 mother–child pairs from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project. Mothers reported the IBQ-R at 3 and 6 months, and the ECBQ at 18 and 36 months, from which measures of dysregulation were extracted. Mothers' self-reported symptoms of depression on the CES-D at 24–36 weeks of gestation, and at 6, 12, 24 and 36 months postnatal. 5-HTTLPR genotype was extracted from buccal swabs. Mixed-model and confirmatory analyses were conducted. Results Prenatal depression and 5-HTTLPR interacted to predict dysregulation from 3 to 36 months, within a model of strong differential susceptibility. Conclusion Children with S or LG alleles, when exposed to prenatal depression, have higher levels of dysregulation, and when exposed to lower or little prenatal depression, have higher capacity for regulation. Our findings support efforts to identify, support and treat prenatal depression. En ligne : http://dx.doi.org/10.1111/jcpp.12246 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=259
in Journal of Child Psychology and Psychiatry > 56-1 (January 2015) . - p.21-29[article] Prenatal depression and 5-HTTLPR interact to predict dysregulation from 3 to 36 months – A differential susceptibility model [Texte imprimé et/ou numérique] / Vanessa BABINEAU, Auteur ; Cathryn Gordon GREEN, Auteur ; Alexis JOLICOEUR-MARTINEAU, Auteur ; Andrée-Anne BOUVETTE-TURCOT, Auteur ; Klaus MINDE, Auteur ; Roberto SASSI, Auteur ; Martin ST-ANDRÉ, Auteur ; Normand J. CARREY, Auteur ; Leslie ATKINSON, Auteur ; James L. KENNEDY, Auteur ; John LYDON, Auteur ; Meir STEINER, Auteur ; Helene GAUDREAU, Auteur ; Robert LEVITAN, Auteur ; Michael MEANEY, Auteur ; Ashley WAZANA, Auteur ; THE MAVAN PROJECT,, Auteur . - p.21-29.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 56-1 (January 2015) . - p.21-29
Mots-clés : Child development emotional dysregulation gene–environment interaction (GxE) longitudinal studies maternal depression Prenatal Index. décimale : PER Périodiques Résumé : Background Childhood dysregulation, which reflects deficits in the capacity to regulate or control one's thoughts, emotions and behaviours, is associated with psychopathology throughout childhood and into adulthood. Exposures to adversity during the prenatal period, including prenatal depression, can influence the development of dysregulation, and a number of candidate genes have been suggested as moderators of prenatal exposure, including polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR). We examined whether prenatal depression and child 5-HTTLPR interact to predict childhood dysregulation. Method Sample of N = 213 mother–child pairs from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project. Mothers reported the IBQ-R at 3 and 6 months, and the ECBQ at 18 and 36 months, from which measures of dysregulation were extracted. Mothers' self-reported symptoms of depression on the CES-D at 24–36 weeks of gestation, and at 6, 12, 24 and 36 months postnatal. 5-HTTLPR genotype was extracted from buccal swabs. Mixed-model and confirmatory analyses were conducted. Results Prenatal depression and 5-HTTLPR interacted to predict dysregulation from 3 to 36 months, within a model of strong differential susceptibility. Conclusion Children with S or LG alleles, when exposed to prenatal depression, have higher levels of dysregulation, and when exposed to lower or little prenatal depression, have higher capacity for regulation. Our findings support efforts to identify, support and treat prenatal depression. En ligne : http://dx.doi.org/10.1111/jcpp.12246 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=259