Editorial: gene–environment interplay in child psychology and psychiatry – challenges and ways forward / Stephen A. PETRILL in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1029-1029 Titre : Editorial: gene–environment interplay in child psychology and psychiatry – challenges and ways forward Type de document : Texte imprimé et/ou numérique Auteurs : Stephen A. PETRILL, Auteur ; Christopher W. BARTLETT, Auteur ; Clancy BLAIR, Auteur Article en page(s) : p.1029-1029 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This special issue in the Journal of Child Psychology and Psychiatry presents several invited articles examining gene–environment interplay in child development and psychopathology. Models of gene–environment interplay have been exhaustively discussed in the literature, including an important contribution by Rutter, Moffitt and Caspi (2006) published in this journal. En ligne : http://dx.doi.org/10.1111/jcpp.12133 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Editorial: gene–environment interplay in child psychology and psychiatry – challenges and ways forward [Texte imprimé et/ou numérique] / Stephen A. PETRILL, Auteur ; Christopher W. BARTLETT, Auteur ; Clancy BLAIR, Auteur . - p.1029-1029. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1029-1029 Index. décimale : PER Périodiques Résumé : This special issue in the Journal of Child Psychology and Psychiatry presents several invited articles examining gene–environment interplay in child development and psychopathology. Models of gene–environment interplay have been exhaustively discussed in the literature, including an important contribution by Rutter, Moffitt and Caspi (2006) published in this journal. En ligne : http://dx.doi.org/10.1111/jcpp.12133 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Gene × smoking interactions on human brain gene expression: finding common mechanisms in adolescents and adults / Samuel L. WOLOCK in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1109-1119 Titre : Gene × smoking interactions on human brain gene expression: finding common mechanisms in adolescents and adults Type de document : Texte imprimé et/ou numérique Auteurs : Samuel L. WOLOCK, Auteur ; Andrew YATES, Auteur ; Stephen A. PETRILL, Auteur ; Jason W. BOHLAND, Auteur ; Clancy BLAIR, Auteur ; Ning LI, Auteur ; Raghu MACHIRAJU, Auteur ; Kun HUANG, Auteur ; Christopher W. BARTLETT, Auteur Article en page(s) : p.1109-1119 Langues : Anglais (eng) Mots-clés : Genetics  environment  brain development  developmental psychopathology Index. décimale : PER Périodiques Résumé : Background Numerous studies have examined gene × environment interactions (G × E) in cognitive and behavioral domains. However, these studies have been limited in that they have not been able to directly assess differential patterns of gene expression in the human brain. Here, we assessed G × E interactions using two publically available datasets to assess if DNA variation is associated with post-mortem brain gene expression changes based on smoking behavior, a biobehavioral construct that is part of a complex system of genetic and environmental influences. Methods We conducted an expression quantitative trait locus (eQTL) study on two independent human brain gene expression datasets assessing G × E for selected psychiatric genes and smoking status. We employed linear regression to model the significance of the Gene × Smoking interaction term, followed by meta-analysis across datasets. Results Overall, we observed that the effect of DNA variation on gene expression is moderated by smoking status. Expression of 16 genes was significantly associated with single nucleotide polymorphisms that demonstrated G × E effects. The strongest finding (p = 1.9 × 10?11) was neurexin 3-alpha (NRXN3), a synaptic cell–cell adhesion molecule involved in maintenance of neural connections (such as the maintenance of smoking behavior). Other significant G × E associations include four glutamate genes. Conclusions This is one of the first studies to demonstrate G × E effects within the human brain. In particular, this study implicated NRXN3 in the maintenance of smoking. The effect of smoking on NRXN3 expression and downstream behavior is different based upon SNP genotype, indicating that DNA profiles based on SNPs could be useful in understanding the effects of smoking behaviors. These results suggest that better measurement of psychiatric conditions, and the environment in post-mortem brain studies may yield an important avenue for understanding the biological mechanisms of G × E interactions in psychiatry. En ligne : http://dx.doi.org/10.1111/jcpp.12119 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Gene × smoking interactions on human brain gene expression: finding common mechanisms in adolescents and adults [Texte imprimé et/ou numérique] / Samuel L. WOLOCK, Auteur ; Andrew YATES, Auteur ; Stephen A. PETRILL, Auteur ; Jason W. BOHLAND, Auteur ; Clancy BLAIR, Auteur ; Ning LI, Auteur ; Raghu MACHIRAJU, Auteur ; Kun HUANG, Auteur ; Christopher W. BARTLETT, Auteur . - p.1109-1119. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1109-1119 Mots-clés : Genetics  environment  brain development  developmental psychopathology Index. décimale : PER Périodiques Résumé : Background Numerous studies have examined gene × environment interactions (G × E) in cognitive and behavioral domains. However, these studies have been limited in that they have not been able to directly assess differential patterns of gene expression in the human brain. Here, we assessed G × E interactions using two publically available datasets to assess if DNA variation is associated with post-mortem brain gene expression changes based on smoking behavior, a biobehavioral construct that is part of a complex system of genetic and environmental influences. Methods We conducted an expression quantitative trait locus (eQTL) study on two independent human brain gene expression datasets assessing G × E for selected psychiatric genes and smoking status. We employed linear regression to model the significance of the Gene × Smoking interaction term, followed by meta-analysis across datasets. Results Overall, we observed that the effect of DNA variation on gene expression is moderated by smoking status. Expression of 16 genes was significantly associated with single nucleotide polymorphisms that demonstrated G × E effects. The strongest finding (p = 1.9 × 10?11) was neurexin 3-alpha (NRXN3), a synaptic cell–cell adhesion molecule involved in maintenance of neural connections (such as the maintenance of smoking behavior). Other significant G × E associations include four glutamate genes. Conclusions This is one of the first studies to demonstrate G × E effects within the human brain. In particular, this study implicated NRXN3 in the maintenance of smoking. The effect of smoking on NRXN3 expression and downstream behavior is different based upon SNP genotype, indicating that DNA profiles based on SNPs could be useful in understanding the effects of smoking behaviors. These results suggest that better measurement of psychiatric conditions, and the environment in post-mortem brain studies may yield an important avenue for understanding the biological mechanisms of G × E interactions in psychiatry. En ligne : http://dx.doi.org/10.1111/jcpp.12119 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Who is afraid of math? Two sources of genetic variance for mathematical anxiety / Zhe WANG in Journal of Child Psychology and Psychiatry, 55-9 (September 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-9 (September 2014) . - p.1056-1064 Titre : Who is afraid of math? Two sources of genetic variance for mathematical anxiety Type de document : Texte imprimé et/ou numérique Auteurs : Zhe WANG, Auteur ; Sara Ann HART, Auteur ; Yulia KOVAS, Auteur ; Sarah LUKOWSKI, Auteur ; Brooke SODEN, Auteur ; Lee A. THOMPSON, Auteur ; Robert PLOMIN, Auteur ; Gráinne MCLOUGHLIN, Auteur ; Christopher W. BARTLETT, Auteur ; Ian M. LYONS, Auteur ; Stephen A. PETRILL, Auteur Article en page(s) : p.1056-1064 Langues : Anglais (eng) Mots-clés : Mathematical anxiety  general anxiety  math cognition  quantitative genetics Index. décimale : PER Périodiques Résumé : Background Emerging work suggests that academic achievement may be influenced by the management of affect as well as through efficient information processing of task demands. In particular, mathematical anxiety has attracted recent attention because of its damaging psychological effects and potential associations with mathematical problem solving and achievement. This study investigated the genetic and environmental factors contributing to the observed differences in the anxiety people feel when confronted with mathematical tasks. In addition, the genetic and environmental mechanisms that link mathematical anxiety with math cognition and general anxiety were also explored. Methods Univariate and multivariate quantitative genetic models were conducted in a sample of 514 12-year-old twin siblings. Results Genetic factors accounted for roughly 40% of the variation in mathematical anxiety, with the remaining being accounted for by child-specific environmental factors. Multivariate genetic analyses suggested that mathematical anxiety was influenced by the genetic and nonfamilial environmental risk factors associated with general anxiety and additional independent genetic influences associated with math-based problem solving. Conclusions The development of mathematical anxiety may involve not only exposure to negative experiences with mathematics, but also likely involves genetic risks related to both anxiety and math cognition. These results suggest that integrating cognitive and affective domains may be particularly important for mathematics and may extend to other areas of academic achievement. En ligne : http://dx.doi.org/10.1111/jcpp.12224 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=238 [article] Who is afraid of math? Two sources of genetic variance for mathematical anxiety [Texte imprimé et/ou numérique] / Zhe WANG, Auteur ; Sara Ann HART, Auteur ; Yulia KOVAS, Auteur ; Sarah LUKOWSKI, Auteur ; Brooke SODEN, Auteur ; Lee A. THOMPSON, Auteur ; Robert PLOMIN, Auteur ; Gráinne MCLOUGHLIN, Auteur ; Christopher W. BARTLETT, Auteur ; Ian M. LYONS, Auteur ; Stephen A. PETRILL, Auteur . - p.1056-1064. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 55-9 (September 2014) . - p.1056-1064 Mots-clés : Mathematical anxiety  general anxiety  math cognition  quantitative genetics Index. décimale : PER Périodiques Résumé : Background Emerging work suggests that academic achievement may be influenced by the management of affect as well as through efficient information processing of task demands. In particular, mathematical anxiety has attracted recent attention because of its damaging psychological effects and potential associations with mathematical problem solving and achievement. This study investigated the genetic and environmental factors contributing to the observed differences in the anxiety people feel when confronted with mathematical tasks. In addition, the genetic and environmental mechanisms that link mathematical anxiety with math cognition and general anxiety were also explored. Methods Univariate and multivariate quantitative genetic models were conducted in a sample of 514 12-year-old twin siblings. Results Genetic factors accounted for roughly 40% of the variation in mathematical anxiety, with the remaining being accounted for by child-specific environmental factors. Multivariate genetic analyses suggested that mathematical anxiety was influenced by the genetic and nonfamilial environmental risk factors associated with general anxiety and additional independent genetic influences associated with math-based problem solving. Conclusions The development of mathematical anxiety may involve not only exposure to negative experiences with mathematics, but also likely involves genetic risks related to both anxiety and math cognition. These results suggest that integrating cognitive and affective domains may be particularly important for mathematics and may extend to other areas of academic achievement. En ligne : http://dx.doi.org/10.1111/jcpp.12224 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=238

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