5HTT genotype moderates the influence of early institutional deprivation on emotional problems in adolescence: evidence from the English and Romanian Adoptee (ERA) study / Robert KUMSTA in Journal of Child Psychology and Psychiatry, 51-7 (July 2010)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 51-7 (July 2010) . - p.755-762 Titre : 5HTT genotype moderates the influence of early institutional deprivation on emotional problems in adolescence: evidence from the English and Romanian Adoptee (ERA) study Type de document : texte imprimé Auteurs : Robert KUMSTA, Auteur ; Michael RUTTER, Auteur ; Jana KREPPNER, Auteur ; Celia BECKETT, Auteur ; Jenny CASTLE, Auteur ; Suzanne E. STEVENS, Auteur ; Edmund J.S. SONUGA-BARKE, Auteur ; Keeley-Joanne BROOKES, Auteur ; Wolff SCHLOTZ, Auteur Année de publication : 2010 Article en page(s) : p.755-762 Langues : Anglais (eng) Mots-clés : Early-institutional-deprivation prospective-longitudinal-study gene–environment-interactions 5-HTTLPR depression Index. décimale : PER Périodiques Résumé : Background: A common polymorphism in the serotonin transporter gene (SLC6A4, 5HTT) has been repeatedly shown to moderate the influence of childhood adversity and stressful life events on the development of psychopathology. Using data from the English and Romanian Adoptee Study, a prospective-longitudinal study of individuals (n = 125) exposed to severe early institutional deprivation (ID), we tested whether the effect of ID on adolescent emotional problems is moderated by 5HTT genotype and stressful life events in adolescence. Methods: Emotional problems were assessed using questionnaire data (age 11), and on the basis of the CAPA diagnostic interview (age 15). Additionally, the number of stressful life events was measured. Results: There was a significant effect for genotype (p = .003) and a gene × environment interaction (p = .008) that was independent of age at testing. Carriers of the s/l and s/s genotype who experienced severe ID showed the highest emotional problem scores, while l/l homozygotes in the severe ID group showed the lowest overall levels. Furthermore, s/s carriers in the severe ID group who experienced a high number of stressful life events between 11 and 15 years had the largest increases in emotional problem scores, while a low number of stressful life events was associated with the largest decrease (4-way interaction: p = .05). Conclusions: The effects of severe early ID on emotional problems in adolescence are moderated by 5HTT genotype, and influenced by stressful life events in adolescence. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02249.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=101 [article] 5HTT genotype moderates the influence of early institutional deprivation on emotional problems in adolescence: evidence from the English and Romanian Adoptee (ERA) study [texte imprimé] / Robert KUMSTA, Auteur ; Michael RUTTER, Auteur ; Jana KREPPNER, Auteur ; Celia BECKETT, Auteur ; Jenny CASTLE, Auteur ; Suzanne E. STEVENS, Auteur ; Edmund J.S. SONUGA-BARKE, Auteur ; Keeley-Joanne BROOKES, Auteur ; Wolff SCHLOTZ, Auteur . - 2010 . - p.755-762. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 51-7 (July 2010) . - p.755-762 Mots-clés : Early-institutional-deprivation prospective-longitudinal-study gene–environment-interactions 5-HTTLPR depression Index. décimale : PER Périodiques Résumé : Background: A common polymorphism in the serotonin transporter gene (SLC6A4, 5HTT) has been repeatedly shown to moderate the influence of childhood adversity and stressful life events on the development of psychopathology. Using data from the English and Romanian Adoptee Study, a prospective-longitudinal study of individuals (n = 125) exposed to severe early institutional deprivation (ID), we tested whether the effect of ID on adolescent emotional problems is moderated by 5HTT genotype and stressful life events in adolescence. Methods: Emotional problems were assessed using questionnaire data (age 11), and on the basis of the CAPA diagnostic interview (age 15). Additionally, the number of stressful life events was measured. Results: There was a significant effect for genotype (p = .003) and a gene × environment interaction (p = .008) that was independent of age at testing. Carriers of the s/l and s/s genotype who experienced severe ID showed the highest emotional problem scores, while l/l homozygotes in the severe ID group showed the lowest overall levels. Furthermore, s/s carriers in the severe ID group who experienced a high number of stressful life events between 11 and 15 years had the largest increases in emotional problem scores, while a low number of stressful life events was associated with the largest decrease (4-way interaction: p = .05). Conclusions: The effects of severe early ID on emotional problems in adolescence are moderated by 5HTT genotype, and influenced by stressful life events in adolescence. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02249.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=101

The dopamine receptor D4 7-repeat allele and prenatal smoking in ADHD-affected children and their unaffected siblings: no gene–environment interaction / Marieke E. ALTINK in Journal of Child Psychology and Psychiatry, 49-10 (October 2008)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 49-10 (October 2008) . - p.1053-1060 Titre : The dopamine receptor D4 7-repeat allele and prenatal smoking in ADHD-affected children and their unaffected siblings: no gene–environment interaction Type de document : texte imprimé Auteurs : Marieke E. ALTINK, Auteur ; Joseph A. SERGEANT, Auteur ; Wai CHEN, Auteur ; Keeley-Joanne BROOKES, Auteur ; Richard ANNEY, Auteur ; Ellen A. FLIERS, Auteur ; Dorine I E. SLAATS-WILLEMSE, Auteur ; Barbara FRANKE, Auteur ; Alejandro ARIAS-VASQUEZ, Auteur ; Margaret J. THOMPSON, Auteur ; Michael GILL, Auteur ; Cathelijne J.M. BUSCHGENS, Auteur ; Nanda N. ROMMELSE, Auteur ; Jan K. BUITELAAR, Auteur ; Philip ASHERSON, Auteur ; Stephen V. FARAONE, Auteur ; Edmund J.S. SONUGA-BARKE, Auteur ; Aisling MULLIGAN, Auteur Année de publication : 2008 Article en page(s) : p.1053-1060 Langues : Anglais (eng) Mots-clés : Dopamine-receptor-D4-gene attention-deficit-hyperactivity-disorder-(ADHD) maternal-smoking-during-pregnancy gene-by-environment-interaction Index. décimale : PER Périodiques Résumé : Background: The dopamine receptor D4 (DRD4) 7-repeat allele and maternal smoking during pregnancy are both considered as risk factors in the aetiology of attention deficit hyperactivity disorder (ADHD), but few studies have been conducted on their interactive effects in causing ADHD. The purpose of this study is to examine the gene by environment (G×E) interaction of the DRD4 7-repeat allele and smoking during pregnancy on ADHD and oppositional behavior in families from the International Multicenter ADHD Genetics project; and further, to test the hypothesis that the direction of effect of the DRD4 7-repeat allele differs between ADHD affected and unaffected children. Methods: Linear mixed models were used to assess main and interactive effects of the DRD4 7-repeat allele and smoking during pregnancy in 539 ADHD-affected children and their 407 unaffected siblings, aged 6–17 years. Results: There was some evidence pointing to differential effects of the DRD4 7-repeat allele on ADHD and oppositional symptoms in the affected (fewer symptoms) and unaffected children (increasing ADHD symptoms of teacher ratings). Affected children were more often exposed to prenatal smoking than unaffected children. There were limited main effects of prenatal smoking on severity of symptoms. Given the number of tests performed, no indication was found for G×E interactions. Conclusion: Despite the large sample size, no G×E interactions were found. The impact of the DRD4 7-repeat allele might differ, depending on affected status and rater. This finding is discussed in terms of differences in the activity of the dopaminergic system and of different genes involved in rater-specific behaviors. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2008.01998.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=606 [article] The dopamine receptor D4 7-repeat allele and prenatal smoking in ADHD-affected children and their unaffected siblings: no gene–environment interaction [texte imprimé] / Marieke E. ALTINK, Auteur ; Joseph A. SERGEANT, Auteur ; Wai CHEN, Auteur ; Keeley-Joanne BROOKES, Auteur ; Richard ANNEY, Auteur ; Ellen A. FLIERS, Auteur ; Dorine I E. SLAATS-WILLEMSE, Auteur ; Barbara FRANKE, Auteur ; Alejandro ARIAS-VASQUEZ, Auteur ; Margaret J. THOMPSON, Auteur ; Michael GILL, Auteur ; Cathelijne J.M. BUSCHGENS, Auteur ; Nanda N. ROMMELSE, Auteur ; Jan K. BUITELAAR, Auteur ; Philip ASHERSON, Auteur ; Stephen V. FARAONE, Auteur ; Edmund J.S. SONUGA-BARKE, Auteur ; Aisling MULLIGAN, Auteur . - 2008 . - p.1053-1060. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 49-10 (October 2008) . - p.1053-1060 Mots-clés : Dopamine-receptor-D4-gene attention-deficit-hyperactivity-disorder-(ADHD) maternal-smoking-during-pregnancy gene-by-environment-interaction Index. décimale : PER Périodiques Résumé : Background: The dopamine receptor D4 (DRD4) 7-repeat allele and maternal smoking during pregnancy are both considered as risk factors in the aetiology of attention deficit hyperactivity disorder (ADHD), but few studies have been conducted on their interactive effects in causing ADHD. The purpose of this study is to examine the gene by environment (G×E) interaction of the DRD4 7-repeat allele and smoking during pregnancy on ADHD and oppositional behavior in families from the International Multicenter ADHD Genetics project; and further, to test the hypothesis that the direction of effect of the DRD4 7-repeat allele differs between ADHD affected and unaffected children. Methods: Linear mixed models were used to assess main and interactive effects of the DRD4 7-repeat allele and smoking during pregnancy in 539 ADHD-affected children and their 407 unaffected siblings, aged 6–17 years. Results: There was some evidence pointing to differential effects of the DRD4 7-repeat allele on ADHD and oppositional symptoms in the affected (fewer symptoms) and unaffected children (increasing ADHD symptoms of teacher ratings). Affected children were more often exposed to prenatal smoking than unaffected children. There were limited main effects of prenatal smoking on severity of symptoms. Given the number of tests performed, no indication was found for G×E interactions. Conclusion: Despite the large sample size, no G×E interactions were found. The impact of the DRD4 7-repeat allele might differ, depending on affected status and rater. This finding is discussed in terms of differences in the activity of the dopaminergic system and of different genes involved in rater-specific behaviors. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2008.01998.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=606

The role of circadian rhythms and sleep in the aetiology of autism spectrum disorder and attention-deficit/hyperactivity disorder: New evidence from bidirectional two-sample Mendelian randomization analysis / Xiaotian DAI in Autism, 29-1 (January 2025)  

Public ISBD [article]  inAutism > 29-1 (January 2025) . - p.76-86 Titre : The role of circadian rhythms and sleep in the aetiology of autism spectrum disorder and attention-deficit/hyperactivity disorder: New evidence from bidirectional two-sample Mendelian randomization analysis Type de document : texte imprimé Auteurs : Xiaotian DAI, Auteur ; Gareth J. WILLIAMS, Auteur ; John A. GROEGER, Auteur ; Gary JONES, Auteur ; Keeley-Joanne BROOKES, Auteur ; Wei ZHOU, Auteur ; Jing HUA, Auteur ; Wenchong DU, Auteur Article en page(s) : p.76-86 Langues : Anglais (eng) Mots-clés : attention-deficit/hyperactivity disorder  autism spectrum disorder  chronotype  circadian rhythm  Mendelian randomization  sleep disorder Index. décimale : PER Périodiques Résumé : Increasing evidence highlights the role of disrupted circadian rhythms in the neural dysfunctions and sleep disturbances observed in autism spectrum disorder and attention-deficit/hyperactivity disorder. However, the causality and directionality of these associations remain unclear. In this study, we employed a bidirectional two-sample Mendelian randomization framework, leveraging genome-wide association study data from the UK Biobank (n = 85,670) and FinnGen (n = 377,277). Genetic variants served as instrumental variables to infer causation, and objective accelerometer-derived metrics identified circadian rhythm and sleep genetic instruments. The results showed that the timing of the most active 10 h was significantly linked to higher odds of autism spectrum disorder and attention-deficit/hyperactivity disorder. Independently, higher sleep efficiency predicted a lower risk of autism spectrum disorder, while attention-deficit/hyperactivity disorder was linked to an increase in nocturnal sleep episodes. Heterogeneity and sensitivity analyses confirmed these findings. Our study establishes causal links between circadian alterations and autism spectrum disorder and attention-deficit/hyperactivity disorder, distinguishing the independent and protective role of sleep efficiency in autism spectrum disorder from circadian rhythms. In attention-deficit/hyperactivity disorder, however, disrupted sleep appears as a consequence, not a cause. These insights highlight divergent interactions with sleep factors in autism spectrum disorder and attention-deficit/hyperactivity disorder, laying the groundwork for tailored therapeutic strategies that recognize the distinct influences of sleep quality and circadian rhythms in each disorder.Lay abstractResearch shows that people with autism spectrum disorder and attention-deficit/hyperactivity disorder often have sleep issues and problems with the body?s natural daily rhythms, known as circadian rhythms. By exploring the genetic variants associated with these rhythms and the conditions, this study reveals that these rhythm changes and sleep patterns are directly linked to autism spectrum disorder and attention-deficit/hyperactivity disorder. It found that the timing of one?s most active hours can increase the likelihood of having both autism spectrum disorder and attention-deficit/hyperactivity disorder. Importantly, it also shows that good sleep quality might protect against autism spectrum disorder, while disturbed sleep in people with attention-deficit/hyperactivity disorder seems to be a result rather than the cause of the condition. This understanding can help doctors and researchers develop better treatment approaches that focus on the specific ways sleep and body rhythms affect those with autism spectrum disorder and attention-deficit/hyperactivity disorder, considering their unique associations with circadian rhythms and sleep patterns. Understanding these unique links can lead to more effective, personalized care for those affected by these conditions. En ligne : https://dx.doi.org/10.1177/13623613241258546 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=544 [article] The role of circadian rhythms and sleep in the aetiology of autism spectrum disorder and attention-deficit/hyperactivity disorder: New evidence from bidirectional two-sample Mendelian randomization analysis [texte imprimé] / Xiaotian DAI, Auteur ; Gareth J. WILLIAMS, Auteur ; John A. GROEGER, Auteur ; Gary JONES, Auteur ; Keeley-Joanne BROOKES, Auteur ; Wei ZHOU, Auteur ; Jing HUA, Auteur ; Wenchong DU, Auteur . - p.76-86. Langues : Anglais (eng) in Autism > 29-1 (January 2025) . - p.76-86 Mots-clés : attention-deficit/hyperactivity disorder  autism spectrum disorder  chronotype  circadian rhythm  Mendelian randomization  sleep disorder Index. décimale : PER Périodiques Résumé : Increasing evidence highlights the role of disrupted circadian rhythms in the neural dysfunctions and sleep disturbances observed in autism spectrum disorder and attention-deficit/hyperactivity disorder. However, the causality and directionality of these associations remain unclear. In this study, we employed a bidirectional two-sample Mendelian randomization framework, leveraging genome-wide association study data from the UK Biobank (n = 85,670) and FinnGen (n = 377,277). Genetic variants served as instrumental variables to infer causation, and objective accelerometer-derived metrics identified circadian rhythm and sleep genetic instruments. The results showed that the timing of the most active 10 h was significantly linked to higher odds of autism spectrum disorder and attention-deficit/hyperactivity disorder. Independently, higher sleep efficiency predicted a lower risk of autism spectrum disorder, while attention-deficit/hyperactivity disorder was linked to an increase in nocturnal sleep episodes. Heterogeneity and sensitivity analyses confirmed these findings. Our study establishes causal links between circadian alterations and autism spectrum disorder and attention-deficit/hyperactivity disorder, distinguishing the independent and protective role of sleep efficiency in autism spectrum disorder from circadian rhythms. In attention-deficit/hyperactivity disorder, however, disrupted sleep appears as a consequence, not a cause. These insights highlight divergent interactions with sleep factors in autism spectrum disorder and attention-deficit/hyperactivity disorder, laying the groundwork for tailored therapeutic strategies that recognize the distinct influences of sleep quality and circadian rhythms in each disorder.Lay abstractResearch shows that people with autism spectrum disorder and attention-deficit/hyperactivity disorder often have sleep issues and problems with the body?s natural daily rhythms, known as circadian rhythms. By exploring the genetic variants associated with these rhythms and the conditions, this study reveals that these rhythm changes and sleep patterns are directly linked to autism spectrum disorder and attention-deficit/hyperactivity disorder. It found that the timing of one?s most active hours can increase the likelihood of having both autism spectrum disorder and attention-deficit/hyperactivity disorder. Importantly, it also shows that good sleep quality might protect against autism spectrum disorder, while disturbed sleep in people with attention-deficit/hyperactivity disorder seems to be a result rather than the cause of the condition. This understanding can help doctors and researchers develop better treatment approaches that focus on the specific ways sleep and body rhythms affect those with autism spectrum disorder and attention-deficit/hyperactivity disorder, considering their unique associations with circadian rhythms and sleep patterns. Understanding these unique links can lead to more effective, personalized care for those affected by these conditions. En ligne : https://dx.doi.org/10.1177/13623613241258546 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=544

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