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Complex effects of dyslexia risk factors account for ADHD traits: evidence from two independent samples / Sara MASCHERETTI in Journal of Child Psychology and Psychiatry, 58-1 (January 2017)
[article]
Titre : Complex effects of dyslexia risk factors account for ADHD traits: evidence from two independent samples Type de document : Texte imprimé et/ou numérique Auteurs : Sara MASCHERETTI, Auteur ; Vittoria TREZZI, Auteur ; Roberto GIORDA, Auteur ; Michel BOIVIN, Auteur ; Vickie PLOURDE, Auteur ; Frank VITARO, Auteur ; Mara BRENDGEN, Auteur ; Ginette DIONNE, Auteur ; Cecilia MARINO, Auteur Article en page(s) : p.75-82 Langues : Anglais (eng) Mots-clés : Developmental dyslexia attention deficit/hyperactivity disorder association study gene-by-environment interaction gene-by-gene interaction pleiotropy Index. décimale : PER Périodiques Résumé : Background Developmental dyslexia (DD) and attention deficit/hyperactivity disorder (ADHD) are among the most common neurodevelopmental disorders, whose etiology involves multiple risk factors. DD and ADHD co-occur in the same individuals much more often than would be expected by chance. Several studies have found significant bivariate heritability, and specific genes associated with either DD or ADHD have been investigated for association in the other disorder. Moreover, there are likely to be gene-by-gene and gene-by-environment interaction effects (G × G and G × E, respectively) underlying the comorbidity between DD and ADHD. We investigated the pleiotropic effects of 19 SNPs spanning five DD genes (DYX1C1, DCDC2, KIAA0319, ROBO1, and GRIN2B) and seven DD environmental factors (smoke, miscarriage, birth weight, breastfeeding, parental age, socioeconomic status, and parental education) for main, either (a) genetic or (b) environmental, (c) G × G, and (d) G × E upon inattention and hyperactivity/impulsivity. We then attempted replication of these findings in an independent twin cohort. Methods Marker-trait association was analyzed by implementing the Quantitative Transmission Disequilibrium Test (QTDT). Environmental associations were tested by partial correlations. G × G were investigated by a general linear model equation and a family-based association test. G × E were analyzed through a general test for G × E in sib pair-based association analysis of quantitative traits. Results DCDC2-rs793862 was associated with hyperactivity/impulsivity via G × G (KIAA0319) and G × E (miscarriage). Smoke was significantly correlated with hyperactivity/impulsivity. We replicated the DCDC2 × KIAA0319 interaction upon hyperactivity/impulsivity in the twin cohort. Conclusions En ligne : http://dx.doi.org/10.1111/jcpp.12612 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298
in Journal of Child Psychology and Psychiatry > 58-1 (January 2017) . - p.75-82[article] Complex effects of dyslexia risk factors account for ADHD traits: evidence from two independent samples [Texte imprimé et/ou numérique] / Sara MASCHERETTI, Auteur ; Vittoria TREZZI, Auteur ; Roberto GIORDA, Auteur ; Michel BOIVIN, Auteur ; Vickie PLOURDE, Auteur ; Frank VITARO, Auteur ; Mara BRENDGEN, Auteur ; Ginette DIONNE, Auteur ; Cecilia MARINO, Auteur . - p.75-82.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 58-1 (January 2017) . - p.75-82
Mots-clés : Developmental dyslexia attention deficit/hyperactivity disorder association study gene-by-environment interaction gene-by-gene interaction pleiotropy Index. décimale : PER Périodiques Résumé : Background Developmental dyslexia (DD) and attention deficit/hyperactivity disorder (ADHD) are among the most common neurodevelopmental disorders, whose etiology involves multiple risk factors. DD and ADHD co-occur in the same individuals much more often than would be expected by chance. Several studies have found significant bivariate heritability, and specific genes associated with either DD or ADHD have been investigated for association in the other disorder. Moreover, there are likely to be gene-by-gene and gene-by-environment interaction effects (G × G and G × E, respectively) underlying the comorbidity between DD and ADHD. We investigated the pleiotropic effects of 19 SNPs spanning five DD genes (DYX1C1, DCDC2, KIAA0319, ROBO1, and GRIN2B) and seven DD environmental factors (smoke, miscarriage, birth weight, breastfeeding, parental age, socioeconomic status, and parental education) for main, either (a) genetic or (b) environmental, (c) G × G, and (d) G × E upon inattention and hyperactivity/impulsivity. We then attempted replication of these findings in an independent twin cohort. Methods Marker-trait association was analyzed by implementing the Quantitative Transmission Disequilibrium Test (QTDT). Environmental associations were tested by partial correlations. G × G were investigated by a general linear model equation and a family-based association test. G × E were analyzed through a general test for G × E in sib pair-based association analysis of quantitative traits. Results DCDC2-rs793862 was associated with hyperactivity/impulsivity via G × G (KIAA0319) and G × E (miscarriage). Smoke was significantly correlated with hyperactivity/impulsivity. We replicated the DCDC2 × KIAA0319 interaction upon hyperactivity/impulsivity in the twin cohort. Conclusions En ligne : http://dx.doi.org/10.1111/jcpp.12612 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298 Investigating the effects of copy number variants on reading and language performance / A. GIALLUISI in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
[article]
Titre : Investigating the effects of copy number variants on reading and language performance Type de document : Texte imprimé et/ou numérique Auteurs : A. GIALLUISI, Auteur ; A. VISCONTI, Auteur ; E. G. WILLCUTT, Auteur ; S. D. SMITH, Auteur ; B. F. PENNINGTON, Auteur ; M. FALCHI, Auteur ; J. C. DEFRIES, Auteur ; R. K. OLSON, Auteur ; C. FRANCKS, Auteur ; S. E. FISHER, Auteur Article en page(s) : p.17 Langues : Anglais (eng) Mots-clés : Cldrc Copy number variants Developmental dyslexia Family-based GWAS Language Meta-analysis Reading Reading disability Index. décimale : PER Périodiques Résumé : BACKGROUND: Reading and language skills have overlapping genetic bases, most of which are still unknown. Part of the missing heritability may be caused by copy number variants (CNVs). METHODS: In a dataset of children recruited for a history of reading disability (RD, also known as dyslexia) or attention deficit hyperactivity disorder (ADHD) and their siblings, we investigated the effects of CNVs on reading and language performance. First, we called CNVs with PennCNV using signal intensity data from Illumina OmniExpress arrays (~723,000 probes). Then, we computed the correlation between measures of CNV genomic burden and the first principal component (PC) score derived from several continuous reading and language traits, both before and after adjustment for performance IQ. Finally, we screened the genome, probe-by-probe, for association with the PC scores, through two complementary analyses: we tested a binary CNV state assigned for the location of each probe (i.e., CNV+ or CNV-), and we analyzed continuous probe intensity data using FamCNV. RESULTS: No significant correlation was found between measures of CNV burden and PC scores, and no genome-wide significant associations were detected in probe-by-probe screening. Nominally significant associations were detected (p~10(-2)-10(-3)) within CNTN4 (contactin 4) and CTNNA3 (catenin alpha 3). These genes encode cell adhesion molecules with a likely role in neuronal development, and they have been previously implicated in autism and other neurodevelopmental disorders. A further, targeted assessment of candidate CNV regions revealed associations with the PC score (p~0.026-0.045) within CHRNA7 (cholinergic nicotinic receptor alpha 7), which encodes a ligand-gated ion channel and has also been implicated in neurodevelopmental conditions and language impairment. FamCNV analysis detected a region of association (p~10(-2)-10(-4)) within a frequent deletion ~6 kb downstream of ZNF737 (zinc finger protein 737, uncharacterized protein), which was also observed in the association analysis using CNV calls. CONCLUSIONS: These data suggest that CNVs do not underlie a substantial proportion of variance in reading and language skills. Analysis of additional, larger datasets is warranted to further assess the potential effects that we found and to increase the power to detect CNV effects on reading and language. En ligne : http://dx.doi.org/10.1186/s11689-016-9147-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.17[article] Investigating the effects of copy number variants on reading and language performance [Texte imprimé et/ou numérique] / A. GIALLUISI, Auteur ; A. VISCONTI, Auteur ; E. G. WILLCUTT, Auteur ; S. D. SMITH, Auteur ; B. F. PENNINGTON, Auteur ; M. FALCHI, Auteur ; J. C. DEFRIES, Auteur ; R. K. OLSON, Auteur ; C. FRANCKS, Auteur ; S. E. FISHER, Auteur . - p.17.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.17
Mots-clés : Cldrc Copy number variants Developmental dyslexia Family-based GWAS Language Meta-analysis Reading Reading disability Index. décimale : PER Périodiques Résumé : BACKGROUND: Reading and language skills have overlapping genetic bases, most of which are still unknown. Part of the missing heritability may be caused by copy number variants (CNVs). METHODS: In a dataset of children recruited for a history of reading disability (RD, also known as dyslexia) or attention deficit hyperactivity disorder (ADHD) and their siblings, we investigated the effects of CNVs on reading and language performance. First, we called CNVs with PennCNV using signal intensity data from Illumina OmniExpress arrays (~723,000 probes). Then, we computed the correlation between measures of CNV genomic burden and the first principal component (PC) score derived from several continuous reading and language traits, both before and after adjustment for performance IQ. Finally, we screened the genome, probe-by-probe, for association with the PC scores, through two complementary analyses: we tested a binary CNV state assigned for the location of each probe (i.e., CNV+ or CNV-), and we analyzed continuous probe intensity data using FamCNV. RESULTS: No significant correlation was found between measures of CNV burden and PC scores, and no genome-wide significant associations were detected in probe-by-probe screening. Nominally significant associations were detected (p~10(-2)-10(-3)) within CNTN4 (contactin 4) and CTNNA3 (catenin alpha 3). These genes encode cell adhesion molecules with a likely role in neuronal development, and they have been previously implicated in autism and other neurodevelopmental disorders. A further, targeted assessment of candidate CNV regions revealed associations with the PC score (p~0.026-0.045) within CHRNA7 (cholinergic nicotinic receptor alpha 7), which encodes a ligand-gated ion channel and has also been implicated in neurodevelopmental conditions and language impairment. FamCNV analysis detected a region of association (p~10(-2)-10(-4)) within a frequent deletion ~6 kb downstream of ZNF737 (zinc finger protein 737, uncharacterized protein), which was also observed in the association analysis using CNV calls. CONCLUSIONS: These data suggest that CNVs do not underlie a substantial proportion of variance in reading and language skills. Analysis of additional, larger datasets is warranted to further assess the potential effects that we found and to increase the power to detect CNV effects on reading and language. En ligne : http://dx.doi.org/10.1186/s11689-016-9147-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348