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 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] / 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 Auteurs : Alexandria MEYER, Auteur ; Greg HAJCAK, Auteur ; Elizabeth P. 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] / Alexandria MEYER, Auteur ; Greg HAJCAK, Auteur ; Elizabeth P. 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

Hippocampal transcriptome analysis following maternal separation implicates altered RNA processing in a mouse model of fetal alcohol spectrum disorder / Bonnie L.J. ALBERRY in Journal of Neurodevelopmental Disorders, 12 (2020)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 12 (2020) Titre : Hippocampal transcriptome analysis following maternal separation implicates altered RNA processing in a mouse model of fetal alcohol spectrum disorder Type de document : texte imprimé Auteurs : Bonnie L.J. ALBERRY, Auteur ; Christina A. CASTELLANI, Auteur ; Shiva M. SINGH, Auteur Langues : Anglais (eng) Mots-clés : Alcohol Drinking/genetics  Animals  Animals, Newborn  Anxiety  Canada  Disease Models, Animal  Ethanol/administration & dosage/metabolism  Female  Fetal Alcohol Spectrum Disorders/genetics/metabolism  Gene Expression Profiling  Gene Expression Regulation  Hippocampus/metabolism  Maternal Deprivation  Mice  Pregnancy  Prenatal Exposure Delayed Effects/genetics/metabolism  RNA Processing, Post-Transcriptional  Transcriptome  Fetal alcohol spectrum disorder  Gene expression  Hippocampus  Maternal separation  Prenatal alcohol  Wgcna Index. décimale : PER Périodiques Résumé : BACKGROUND: Fetal alcohol spectrum disorders (FASD) are common, seen in 1-5% of the population in the USA and Canada. Children diagnosed with FASD are not likely to remain with their biological parents, facing early maternal separation and foster placements throughout childhood. METHODS: We model FASD in mice via prenatal alcohol exposure and further induce early life stress through maternal separation. We use RNA-seq followed by clustering of expression profiles through weighted gene co-expression network analysis (WGCNA) to analyze transcriptomic changes that result from the treatments. We use reverse transcription qPCR to validate these changes in the mouse hippocampus. RESULTS: We report an association between adult hippocampal gene expression and prenatal ethanol exposure followed by postnatal separation stress that is related to behavioral changes. Expression profile clustering using WGCNA identifies a set of transcripts, module 19, associated with anxiety-like behavior (r = 0.79, p = 0.002) as well as treatment group (r = 0.68, p = 0.015). Genes in this module are overrepresented by genes involved in transcriptional regulation and other pathways related to neurodevelopment. Interestingly, one member of this module, Polr2a, polymerase (RNA) II (DNA directed) polypeptide A, is downregulated by the combination of prenatal ethanol and postnatal stress in an RNA-Seq experiment and qPCR validation (q = 2e-12, p = 0.004, respectively). CONCLUSIONS: Together, transcriptional control in the hippocampus is implicated as a potential underlying mechanism leading to anxiety-like behavior via environmental insults. Further research is required to elucidate the mechanism involved and use this insight towards early diagnosis and amelioration strategies involving children born with FASD. En ligne : https://dx.doi.org/10.1186/s11689-020-09316-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573 [article] Hippocampal transcriptome analysis following maternal separation implicates altered RNA processing in a mouse model of fetal alcohol spectrum disorder [texte imprimé] / Bonnie L.J. ALBERRY, Auteur ; Christina A. CASTELLANI, Auteur ; Shiva M. SINGH, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 12 (2020) Mots-clés : Alcohol Drinking/genetics  Animals  Animals, Newborn  Anxiety  Canada  Disease Models, Animal  Ethanol/administration & dosage/metabolism  Female  Fetal Alcohol Spectrum Disorders/genetics/metabolism  Gene Expression Profiling  Gene Expression Regulation  Hippocampus/metabolism  Maternal Deprivation  Mice  Pregnancy  Prenatal Exposure Delayed Effects/genetics/metabolism  RNA Processing, Post-Transcriptional  Transcriptome  Fetal alcohol spectrum disorder  Gene expression  Hippocampus  Maternal separation  Prenatal alcohol  Wgcna Index. décimale : PER Périodiques Résumé : BACKGROUND: Fetal alcohol spectrum disorders (FASD) are common, seen in 1-5% of the population in the USA and Canada. Children diagnosed with FASD are not likely to remain with their biological parents, facing early maternal separation and foster placements throughout childhood. METHODS: We model FASD in mice via prenatal alcohol exposure and further induce early life stress through maternal separation. We use RNA-seq followed by clustering of expression profiles through weighted gene co-expression network analysis (WGCNA) to analyze transcriptomic changes that result from the treatments. We use reverse transcription qPCR to validate these changes in the mouse hippocampus. RESULTS: We report an association between adult hippocampal gene expression and prenatal ethanol exposure followed by postnatal separation stress that is related to behavioral changes. Expression profile clustering using WGCNA identifies a set of transcripts, module 19, associated with anxiety-like behavior (r = 0.79, p = 0.002) as well as treatment group (r = 0.68, p = 0.015). Genes in this module are overrepresented by genes involved in transcriptional regulation and other pathways related to neurodevelopment. Interestingly, one member of this module, Polr2a, polymerase (RNA) II (DNA directed) polypeptide A, is downregulated by the combination of prenatal ethanol and postnatal stress in an RNA-Seq experiment and qPCR validation (q = 2e-12, p = 0.004, respectively). CONCLUSIONS: Together, transcriptional control in the hippocampus is implicated as a potential underlying mechanism leading to anxiety-like behavior via environmental insults. Further research is required to elucidate the mechanism involved and use this insight towards early diagnosis and amelioration strategies involving children born with FASD. En ligne : https://dx.doi.org/10.1186/s11689-020-09316-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573

Neurodevelopmental alcohol exposure elicits long-term changes to gene expression that alter distinct molecular pathways dependent on timing of exposure / Morgan L. KLEIBER in Journal of Neurodevelopmental Disorders, 5-1 (December 2013)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 5-1 (December 2013) . - p.6 Titre : Neurodevelopmental alcohol exposure elicits long-term changes to gene expression that alter distinct molecular pathways dependent on timing of exposure Type de document : texte imprimé Auteurs : Morgan L. KLEIBER, Auteur ; Katarzyna MANTHA, Auteur ; Randa L. STRINGER, Auteur ; Shiva M. SINGH, Auteur Article en page(s) : p.6 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Maternal alcohol consumption is known to adversely affect fetal neurodevelopment. While it is known that alcohol dose and timing play a role in the cognitive and behavioral changes associated with prenatal alcohol exposure, it is unclear what developmental processes are disrupted that may lead to these phenotypes. METHODS: Mice (n=6 per treatment per developmental time) were exposed to two acute doses of alcohol (5 g/kg) at neurodevelopmental times representing the human first, second, or third trimester equivalent. Mice were reared to adulthood and changes to their adult brain transcriptome were assessed using expression arrays. These were then categorized based on Gene Ontology annotations, canonical pathway associations, and relationships to interacting molecules. RESULTS: The results suggest that ethanol disrupts biological processes that are actively occurring at the time of exposure. These include cell proliferation during trimester one, cell migration and differentiation during trimester two, and cellular communication and neurotransmission during trimester three. Further, although ethanol altered a distinct set of genes depending on developmental timing, many of these show interrelatedness and can be associated with one another via 'hub' molecules and pathways such as those related to huntingtin and brain-derived neurotrophic factor. CONCLUSIONS: These changes to brain gene expression represent a 'molecular footprint' of neurodevelopmental alcohol exposure that is long-lasting and correlates with active processes disrupted at the time of exposure. This study provides further support that there is no neurodevelopmental time when alcohol cannot adversely affect the developing brain. En ligne : http://dx.doi.org/10.1186/1866-1955-5-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=345 [article] Neurodevelopmental alcohol exposure elicits long-term changes to gene expression that alter distinct molecular pathways dependent on timing of exposure [texte imprimé] / Morgan L. KLEIBER, Auteur ; Katarzyna MANTHA, Auteur ; Randa L. STRINGER, Auteur ; Shiva M. SINGH, Auteur . - p.6. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 5-1 (December 2013) . - p.6 Index. décimale : PER Périodiques Résumé : BACKGROUND: Maternal alcohol consumption is known to adversely affect fetal neurodevelopment. While it is known that alcohol dose and timing play a role in the cognitive and behavioral changes associated with prenatal alcohol exposure, it is unclear what developmental processes are disrupted that may lead to these phenotypes. METHODS: Mice (n=6 per treatment per developmental time) were exposed to two acute doses of alcohol (5 g/kg) at neurodevelopmental times representing the human first, second, or third trimester equivalent. Mice were reared to adulthood and changes to their adult brain transcriptome were assessed using expression arrays. These were then categorized based on Gene Ontology annotations, canonical pathway associations, and relationships to interacting molecules. RESULTS: The results suggest that ethanol disrupts biological processes that are actively occurring at the time of exposure. These include cell proliferation during trimester one, cell migration and differentiation during trimester two, and cellular communication and neurotransmission during trimester three. Further, although ethanol altered a distinct set of genes depending on developmental timing, many of these show interrelatedness and can be associated with one another via 'hub' molecules and pathways such as those related to huntingtin and brain-derived neurotrophic factor. CONCLUSIONS: These changes to brain gene expression represent a 'molecular footprint' of neurodevelopmental alcohol exposure that is long-lasting and correlates with active processes disrupted at the time of exposure. This study provides further support that there is no neurodevelopmental time when alcohol cannot adversely affect the developing brain. En ligne : http://dx.doi.org/10.1186/1866-1955-5-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=345

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 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] / 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)  

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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)  

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