[article] 
inJournal of Child Psychology and Psychiatry > 53-3 (March 2012) . - p.243-251

Titre :	Gene by environment interactions influencing reading disability and the inattentive symptom dimension of attention deficit/hyperactivity disorder
Type de document :	Texte imprimé et/ou numérique
Auteurs :	Jenni ROSENBERG, Auteur ; Bruce F. PENNINGTON, Auteur ; Erik G. WILLCUTT, Auteur ; Richard K. OLSON, Auteur
Année de publication :	2012
Article en page(s) :	p.243-251
Langues :	Anglais (eng)
Mots-clés :	Gene  environment  interactions  reading disability  attention deficit/hyperactivity disorder  bioecological  diathesis-stress
Index. décimale :	PER Périodiques
Résumé :	Background:  Reading disability (RD) and attention deficit/hyperactivity disorder (ADHD) are comorbid and genetically correlated, especially the inattentive dimension of ADHD (ADHD-I). However, previous research indicates that RD and ADHD enter into opposite gene by environment (G × E) interactions. Methods:  This study used behavioral genetic methods to replicate these opposite G × E interactions in a sample of same-sex monozygotic and dizygotic twin pairs from the Colorado Learning Disabilities Research Center (CLDRC; DeFries et al., 1997) and to test a genetic hypothesis for why these opposite interactions occur. Results:  We replicated opposite G × E interactions for RD (bioecological) and ADHD-I (diathesis-stress) with parental education in the same sample of participants. The genetic hypothesis for this opposite pattern of interactions is that only genes specific to each disorder enter into these opposite interactions, not the shared genes underlying their comorbidity. To test this hypothesis, we used single models with an exploratory three-way interaction, in which the G × E interactions for each disorder were moderated by comorbidity. Neither three-way interaction was significant. The heritability of RD did not vary as a function of parental education and ADHD-I. Similarly, the heritability of ADHD-I did not vary as a function of parental education and RD. Conclusions:  We documented opposite G × E interactions in RD and ADHD-I in the same overall twin sample, but the explanation for this apparent paradox remains unclear. Examining specific genes and more specific environmental factors may help resolve the paradox.
En ligne :	http://dx.doi.org/10.1111/j.1469-7610.2011.02452.x
Permalink :	https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152

[article] Gene by environment interactions influencing reading disability and the inattentive symptom dimension of attention deficit/hyperactivity disorder [Texte imprimé et/ou numérique] / Jenni ROSENBERG, Auteur ; Bruce F. PENNINGTON, Auteur ; Erik G. WILLCUTT, Auteur ; Richard K. OLSON, Auteur . - 2012 . - p.243-251.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 53-3 (March 2012) . - p.243-251

Mots-clés :	Gene  environment  interactions  reading disability  attention deficit/hyperactivity disorder  bioecological  diathesis-stress
Index. décimale :	PER Périodiques
Résumé :	Background:  Reading disability (RD) and attention deficit/hyperactivity disorder (ADHD) are comorbid and genetically correlated, especially the inattentive dimension of ADHD (ADHD-I). However, previous research indicates that RD and ADHD enter into opposite gene by environment (G × E) interactions. Methods:  This study used behavioral genetic methods to replicate these opposite G × E interactions in a sample of same-sex monozygotic and dizygotic twin pairs from the Colorado Learning Disabilities Research Center (CLDRC; DeFries et al., 1997) and to test a genetic hypothesis for why these opposite interactions occur. Results:  We replicated opposite G × E interactions for RD (bioecological) and ADHD-I (diathesis-stress) with parental education in the same sample of participants. The genetic hypothesis for this opposite pattern of interactions is that only genes specific to each disorder enter into these opposite interactions, not the shared genes underlying their comorbidity. To test this hypothesis, we used single models with an exploratory three-way interaction, in which the G × E interactions for each disorder were moderated by comorbidity. Neither three-way interaction was significant. The heritability of RD did not vary as a function of parental education and ADHD-I. Similarly, the heritability of ADHD-I did not vary as a function of parental education and RD. Conclusions:  We documented opposite G × E interactions in RD and ADHD-I in the same overall twin sample, but the explanation for this apparent paradox remains unclear. Examining specific genes and more specific environmental factors may help resolve the paradox.
En ligne :	http://dx.doi.org/10.1111/j.1469-7610.2011.02452.x
Permalink :	https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152