Child dopamine active transporter 1 genotype and parenting: Evidence for evocative gene–environment correlations / Elizabeth P. HAYDEN in Development and Psychopathology, 25-1 (February 2013)  

Public ISBD [article]  inDevelopment and Psychopathology > 25-1 (February 2013) . - p.163-173 Titre : Child dopamine active transporter 1 genotype and parenting: Evidence for evocative gene–environment correlations Type de document : Texte imprimé et/ou numérique Auteurs : Elizabeth P. HAYDEN, Auteur ; Brigitte HANNA, Auteur ; Haroon I. SHEIKH, Auteur ; Rebecca S. LAPTOOK, Auteur ; Jiyon KIM, Auteur ; Shiva M. SINGH, Auteur ; Daniel N. KLEIN, Auteur Article en page(s) : p.163-173 Index. décimale : PER Périodiques Résumé : The dopamine active transporter 1 (DAT1) gene is implicated in psychopathology risk. Although the processes by which this gene exerts its effects on risk are poorly understood, a small body of research suggests that the DAT1 gene influences early emerging negative emotionality, a marker of children's psychopathology risk. As child negative emotionality evokes negative parenting practices, the DAT1 gene may also play a role in gene–environment correlations. To test this model, children (N = 365) were genotyped for the DAT1 gene and participated in standardized parent–child interaction tasks with their primary caregiver. The DAT1 gene 9-repeat variant was associated with child negative affect expressed toward the parent during parent–child interactions, and parents of children with a 9-repeat allele exhibited more hostility and lower guidance/engagement than parents of children without a 9-repeat allele. These gene–environment associations were partially mediated by child negative affect toward the parent. The findings implicate a specific polymorphism in eliciting negative parenting, suggesting that evocative associations play a role in elevating children's risk for emotional trajectories toward psychopathology risk. En ligne : http://dx.doi.org/10.1017/S0954579412000971 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=190 [article] Child dopamine active transporter 1 genotype and parenting: Evidence for evocative gene–environment correlations [Texte imprimé et/ou numérique] / Elizabeth P. HAYDEN, Auteur ; Brigitte HANNA, Auteur ; Haroon I. SHEIKH, Auteur ; Rebecca S. LAPTOOK, Auteur ; Jiyon KIM, Auteur ; Shiva M. SINGH, Auteur ; Daniel N. KLEIN, Auteur . - p.163-173. in Development and Psychopathology > 25-1 (February 2013) . - p.163-173 Index. décimale : PER Périodiques Résumé : The dopamine active transporter 1 (DAT1) gene is implicated in psychopathology risk. Although the processes by which this gene exerts its effects on risk are poorly understood, a small body of research suggests that the DAT1 gene influences early emerging negative emotionality, a marker of children's psychopathology risk. As child negative emotionality evokes negative parenting practices, the DAT1 gene may also play a role in gene–environment correlations. To test this model, children (N = 365) were genotyped for the DAT1 gene and participated in standardized parent–child interaction tasks with their primary caregiver. The DAT1 gene 9-repeat variant was associated with child negative affect expressed toward the parent during parent–child interactions, and parents of children with a 9-repeat allele exhibited more hostility and lower guidance/engagement than parents of children without a 9-repeat allele. These gene–environment associations were partially mediated by child negative affect toward the parent. The findings implicate a specific polymorphism in eliciting negative parenting, suggesting that evocative associations play a role in elevating children's risk for emotional trajectories toward psychopathology risk. En ligne : http://dx.doi.org/10.1017/S0954579412000971 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=190

A genetic variant brain-derived neurotrophic factor (BDNF) polymorphism interacts with hostile parenting to predict error-related brain activity and thereby risk for internalizing disorders in children / Alexandria MEYER in Development and Psychopathology, 30-1 (February 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-1 (February 2018) . - p.125-141 Titre : A genetic variant brain-derived neurotrophic factor (BDNF) polymorphism interacts with hostile parenting to predict error-related brain activity and thereby risk for internalizing disorders in children Type de document : Texte imprimé et/ou numérique Auteurs : Alexandria MEYER, Auteur ; Greg HAJCAK, Auteur ; Elizabeth HAYDEN, Auteur ; Haroon I. SHEIKH, Auteur ; Shiva M. SINGH, Auteur ; Daniel N. KLEIN, Auteur Article en page(s) : p.125-141 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The error-related negativity (ERN) is a negative deflection in the event-related potential occurring when individuals make mistakes, and is increased in children with internalizing psychopathology. We recently found that harsh parenting predicts a larger ERN in children, and recent work has suggested that variation in the brain-derived neurotrophic factor (BDNF) gene may moderate the impact of early life adversity. Parents and children completed measures of parenting when children were 3 years old (N = 201); 3 years later, the ERN was measured and diagnostic interviews as well as dimensional symptom measures were completed. We found that harsh parenting predicted an increased ERN only among children with a methionine allele of the BDNF genotype, and evidence of moderated mediation: the ERN mediated the relationship between parenting and internalizing diagnoses and dimensional symptoms only if children had a methionine allele. We tested this model with externalizing disorders, and found that harsh parenting predicted externalizing outcomes, but the ERN did not mediate this association. These findings suggest that harsh parenting predicts both externalizing and internalizing outcomes in children; however, this occurs through different pathways that uniquely implicate error-related brain activity in the development of internalizing disorders. En ligne : https://doi.org/10.1017/S0954579417000517 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=335 [article] A genetic variant brain-derived neurotrophic factor (BDNF) polymorphism interacts with hostile parenting to predict error-related brain activity and thereby risk for internalizing disorders in children [Texte imprimé et/ou numérique] / Alexandria MEYER, Auteur ; Greg HAJCAK, Auteur ; Elizabeth HAYDEN, Auteur ; Haroon I. SHEIKH, Auteur ; Shiva M. SINGH, Auteur ; Daniel N. KLEIN, Auteur . - p.125-141. Langues : Anglais (eng) in Development and Psychopathology > 30-1 (February 2018) . - p.125-141 Index. décimale : PER Périodiques Résumé : The error-related negativity (ERN) is a negative deflection in the event-related potential occurring when individuals make mistakes, and is increased in children with internalizing psychopathology. We recently found that harsh parenting predicts a larger ERN in children, and recent work has suggested that variation in the brain-derived neurotrophic factor (BDNF) gene may moderate the impact of early life adversity. Parents and children completed measures of parenting when children were 3 years old (N = 201); 3 years later, the ERN was measured and diagnostic interviews as well as dimensional symptom measures were completed. We found that harsh parenting predicted an increased ERN only among children with a methionine allele of the BDNF genotype, and evidence of moderated mediation: the ERN mediated the relationship between parenting and internalizing diagnoses and dimensional symptoms only if children had a methionine allele. We tested this model with externalizing disorders, and found that harsh parenting predicted externalizing outcomes, but the ERN did not mediate this association. These findings suggest that harsh parenting predicts both externalizing and internalizing outcomes in children; however, this occurs through different pathways that uniquely implicate error-related brain activity in the development of internalizing disorders. En ligne : https://doi.org/10.1017/S0954579417000517 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=335

Parental depression and child cognitive vulnerability predict children's cortisol reactivity / Elizabeth P. HAYDEN in Development and Psychopathology, 26-4 (Part 2) (November 2014)  

Public ISBD [article]  inDevelopment and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1445-1460 Titre : Parental depression and child cognitive vulnerability predict children's cortisol reactivity Type de document : Texte imprimé et/ou numérique Auteurs : Elizabeth P. HAYDEN, Auteur ; Benjamin L. HANKIN, Auteur ; Sarah V. M. MACKRELL, Auteur ; Haroon I. SHEIKH, Auteur ; Patricia L. JORDAN, Auteur ; David J. A. DOZOIS, Auteur ; Shiva M. SINGH, Auteur ; Thomas M. OLINO, Auteur ; Lisa S. BADANES, Auteur Article en page(s) : p.1445-1460 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Risk for depression is expressed across multiple levels of analysis. For example, parental depression and cognitive vulnerability are known markers of depression risk, but no study has examined their interactive effects on children's cortisol reactivity, a likely mediator of early depression risk. We examined relations across these different levels of vulnerability using cross-sectional and longitudinal methods in two community samples of children. Children were assessed for cognitive vulnerability using self-reports (Study 1; n = 244) and tasks tapping memory and attentional bias (Study 2; n = 205), and their parents were assessed for depression history using structured clinical interviews. In both samples, children participated in standardized stress tasks and cortisol reactivity was assessed. Cross-sectionally and longitudinally, parental depression history and child cognitive vulnerability interacted to predict children's cortisol reactivity; associations between parent depression and elevated child cortisol activity were found when children also showed elevated depressotypic attributions as well as attentional and memory biases. Findings indicate that models of children's emerging depression risk may benefit from the examination of the interactive effects of multiple sources of vulnerability across levels of analysis. En ligne : http://dx.doi.org/10.1017/S0954579414001138 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245 [article] Parental depression and child cognitive vulnerability predict children's cortisol reactivity [Texte imprimé et/ou numérique] / Elizabeth P. HAYDEN, Auteur ; Benjamin L. HANKIN, Auteur ; Sarah V. M. MACKRELL, Auteur ; Haroon I. SHEIKH, Auteur ; Patricia L. JORDAN, Auteur ; David J. A. DOZOIS, Auteur ; Shiva M. SINGH, Auteur ; Thomas M. OLINO, Auteur ; Lisa S. BADANES, Auteur . - p.1445-1460. Langues : Anglais (eng) in Development and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1445-1460 Index. décimale : PER Périodiques Résumé : Risk for depression is expressed across multiple levels of analysis. For example, parental depression and cognitive vulnerability are known markers of depression risk, but no study has examined their interactive effects on children's cortisol reactivity, a likely mediator of early depression risk. We examined relations across these different levels of vulnerability using cross-sectional and longitudinal methods in two community samples of children. Children were assessed for cognitive vulnerability using self-reports (Study 1; n = 244) and tasks tapping memory and attentional bias (Study 2; n = 205), and their parents were assessed for depression history using structured clinical interviews. In both samples, children participated in standardized stress tasks and cortisol reactivity was assessed. Cross-sectionally and longitudinally, parental depression history and child cognitive vulnerability interacted to predict children's cortisol reactivity; associations between parent depression and elevated child cortisol activity were found when children also showed elevated depressotypic attributions as well as attentional and memory biases. Findings indicate that models of children's emerging depression risk may benefit from the examination of the interactive effects of multiple sources of vulnerability across levels of analysis. En ligne : http://dx.doi.org/10.1017/S0954579414001138 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245

The serotonin transporter linked polymorphic region and brain-derived neurotrophic factor valine to methionine at position 66 polymorphisms and maternal history of depression: Associations with cognitive vulnerability to depression in childhood / Elizabeth P. HAYDEN in Development and Psychopathology, 25-3 (August 2013)  

Public ISBD [article]  inDevelopment and Psychopathology > 25-3 (August 2013) . - p.587-598 Titre : The serotonin transporter linked polymorphic region and brain-derived neurotrophic factor valine to methionine at position 66 polymorphisms and maternal history of depression: Associations with cognitive vulnerability to depression in childhood Type de document : Texte imprimé et/ou numérique Auteurs : Elizabeth P. HAYDEN, Auteur ; Thomas M. OLINO, Auteur ; Sara J. BUFFERD, Auteur ; Anna MILLER, Auteur ; Lea R. DOUGHERTY, Auteur ; Haroon I. SHEIKH, Auteur ; Shiva M. SINGH, Auteur ; Daniel N. KLEIN, Auteur Article en page(s) : p.587-598 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Preliminary work indicates that cognitive vulnerability to depression may be associated with variants of the serotonin transporter promoter polymorphism (5-HTTLPR) and the valine to methionine at position 66 (val66met) polymorphism of the brain-derived neurotrophic factor (BDNF) gene; however, existing reports come from small samples. The present study sought to replicate and extend this research in a sample of 375 community-dwelling children and their parents. Following a negative mood induction, children completed a self-referent encoding task tapping memory for positive and negative self-descriptive traits. Consistent with previous work, we found that children with at least one short variant of the 5-HTTLPR had enhanced memory for negative self-descriptive traits. The BDNF val66met polymorphism had no main effect but was moderated by maternal depression, such that children with a BDNF methionine allele had a heightened memory for negative self-descriptive traits when mothers had experienced depression during children's lifetimes; in contrast, children with a methionine allele had low recall of negative traits when mothers had no depression history. The findings provide further support for the notion that the 5-HTTLPR is associated with cognitive markers of depression vulnerability and that the BDNF methionine allele moderates children's sensitivity to contextual factors. En ligne : http://dx.doi.org/10.1017/S0954579413000035 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=210 [article] The serotonin transporter linked polymorphic region and brain-derived neurotrophic factor valine to methionine at position 66 polymorphisms and maternal history of depression: Associations with cognitive vulnerability to depression in childhood [Texte imprimé et/ou numérique] / Elizabeth P. HAYDEN, Auteur ; Thomas M. OLINO, Auteur ; Sara J. BUFFERD, Auteur ; Anna MILLER, Auteur ; Lea R. DOUGHERTY, Auteur ; Haroon I. SHEIKH, Auteur ; Shiva M. SINGH, Auteur ; Daniel N. KLEIN, Auteur . - p.587-598. Langues : Anglais (eng) in Development and Psychopathology > 25-3 (August 2013) . - p.587-598 Index. décimale : PER Périodiques Résumé : Preliminary work indicates that cognitive vulnerability to depression may be associated with variants of the serotonin transporter promoter polymorphism (5-HTTLPR) and the valine to methionine at position 66 (val66met) polymorphism of the brain-derived neurotrophic factor (BDNF) gene; however, existing reports come from small samples. The present study sought to replicate and extend this research in a sample of 375 community-dwelling children and their parents. Following a negative mood induction, children completed a self-referent encoding task tapping memory for positive and negative self-descriptive traits. Consistent with previous work, we found that children with at least one short variant of the 5-HTTLPR had enhanced memory for negative self-descriptive traits. The BDNF val66met polymorphism had no main effect but was moderated by maternal depression, such that children with a BDNF methionine allele had a heightened memory for negative self-descriptive traits when mothers had experienced depression during children's lifetimes; in contrast, children with a methionine allele had low recall of negative traits when mothers had no depression history. The findings provide further support for the notion that the 5-HTTLPR is associated with cognitive markers of depression vulnerability and that the BDNF methionine allele moderates children's sensitivity to contextual factors. En ligne : http://dx.doi.org/10.1017/S0954579413000035 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=210

The serotonin transporter promoter polymorphism moderates the continuity of behavioral inhibition in early childhood / Victoria C. JOHNSON in Development and Psychopathology, 28-4 pt1 (November 2016)  

Public ISBD [article]  inDevelopment and Psychopathology > 28-4 pt1 (November 2016) . - p.1103-1116 Titre : The serotonin transporter promoter polymorphism moderates the continuity of behavioral inhibition in early childhood Type de document : Texte imprimé et/ou numérique Auteurs : Victoria C. JOHNSON, Auteur ; Katie R. KRYSKI, Auteur ; Haroon I. SHEIKH, Auteur ; Heather J. SMITH, Auteur ; Shiva M. SINGH, Auteur ; Elizabeth P. HAYDEN, Auteur Article en page(s) : p.1103-1116 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Persistently elevated behavioral inhibition (BI) in children is a marker of vulnerability to psychopathology. However, little research has considered the joint influences of caregiver and child factors that may moderate the continuity of BI in early childhood, particularly genetic variants that may serve as markers of biological plasticity, such as the serotonin transporter linked polymorphic region (5-HTTLPR). We explored this issue in 371 preschoolers and their caregivers, examining whether parent characteristics (i.e., overinvolvement or anxiety disorder) and child 5-HTTLPR influenced the continuity of BI between ages 3 and 5. Measures were observational ratings of child BI, observational and questionnaire measures of parenting, and parent interviews for anxiety disorder history, and children were genotyped for the 5-HTTLPR. Parent factors did not moderate the association between age 3 and age 5 BI; however, child BI at age 3 interacted with children's 5-HTTLPR variants to predict age 5 BI, such that children with at least one copy of the short allele exhibited less continuity of BI over time relative to children without this putative plasticity variant. Findings are consistent with previous work indicating the 5-HTTLPR short variant increases plasticity to contextual influences, thereby serving to decrease the continuity of BI in early childhood. En ligne : http://dx.doi.org/10.1017/s0954579416000729 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294 [article] The serotonin transporter promoter polymorphism moderates the continuity of behavioral inhibition in early childhood [Texte imprimé et/ou numérique] / Victoria C. JOHNSON, Auteur ; Katie R. KRYSKI, Auteur ; Haroon I. SHEIKH, Auteur ; Heather J. SMITH, Auteur ; Shiva M. SINGH, Auteur ; Elizabeth P. HAYDEN, Auteur . - p.1103-1116. Langues : Anglais (eng) in Development and Psychopathology > 28-4 pt1 (November 2016) . - p.1103-1116 Index. décimale : PER Périodiques Résumé : Persistently elevated behavioral inhibition (BI) in children is a marker of vulnerability to psychopathology. However, little research has considered the joint influences of caregiver and child factors that may moderate the continuity of BI in early childhood, particularly genetic variants that may serve as markers of biological plasticity, such as the serotonin transporter linked polymorphic region (5-HTTLPR). We explored this issue in 371 preschoolers and their caregivers, examining whether parent characteristics (i.e., overinvolvement or anxiety disorder) and child 5-HTTLPR influenced the continuity of BI between ages 3 and 5. Measures were observational ratings of child BI, observational and questionnaire measures of parenting, and parent interviews for anxiety disorder history, and children were genotyped for the 5-HTTLPR. Parent factors did not moderate the association between age 3 and age 5 BI; however, child BI at age 3 interacted with children's 5-HTTLPR variants to predict age 5 BI, such that children with at least one copy of the short allele exhibited less continuity of BI over time relative to children without this putative plasticity variant. Findings are consistent with previous work indicating the 5-HTTLPR short variant increases plasticity to contextual influences, thereby serving to decrease the continuity of BI in early childhood. En ligne : http://dx.doi.org/10.1017/s0954579416000729 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294

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