Childhood adversity and epigenetic regulation of glucocorticoid signaling genes: Associations in children and adults / Audrey R. TYRKA in Development and Psychopathology, 28-4 pt2 (November 2016)  

Public ISBD [article]  inDevelopment and Psychopathology > 28-4 pt2 (November 2016) . - p.1319-1331 Titre : Childhood adversity and epigenetic regulation of glucocorticoid signaling genes: Associations in children and adults Type de document : Texte imprimé et/ou numérique Auteurs : Audrey R. TYRKA, Auteur ; Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur Article en page(s) : p.1319-1331 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Early childhood experiences have lasting effects on development, including the risk for psychiatric disorders. Research examining the biologic underpinnings of these associations has revealed the impact of childhood maltreatment on the physiologic stress response and activity of the hypothalamus–pituitary–adrenal axis. A growing body of literature supports the hypothesis that environmental exposures mediate their biological effects via epigenetic mechanisms. Methylation, which is thought to be the most stable form of epigenetic change, is a likely mechanism by which early life exposures have lasting effects. We present recent evidence related to epigenetic regulation of genes involved in hypothalamus–pituitary–adrenal axis regulation, namely, the glucocorticoid receptor gene (nuclear receptor subfamily 3, group C, member 1 [NR3C1]) and FK506 binding protein 51 gene (FKBP5), after childhood adversity and associations with risk for psychiatric disorders. Implications for the development of interventions and future research are discussed. En ligne : http://dx.doi.org/10.1017/s0954579416000870 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294 [article] Childhood adversity and epigenetic regulation of glucocorticoid signaling genes: Associations in children and adults [Texte imprimé et/ou numérique] / Audrey R. TYRKA, Auteur ; Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur . - p.1319-1331. Langues : Anglais (eng) in Development and Psychopathology > 28-4 pt2 (November 2016) . - p.1319-1331 Index. décimale : PER Périodiques Résumé : Early childhood experiences have lasting effects on development, including the risk for psychiatric disorders. Research examining the biologic underpinnings of these associations has revealed the impact of childhood maltreatment on the physiologic stress response and activity of the hypothalamus–pituitary–adrenal axis. A growing body of literature supports the hypothesis that environmental exposures mediate their biological effects via epigenetic mechanisms. Methylation, which is thought to be the most stable form of epigenetic change, is a likely mechanism by which early life exposures have lasting effects. We present recent evidence related to epigenetic regulation of genes involved in hypothalamus–pituitary–adrenal axis regulation, namely, the glucocorticoid receptor gene (nuclear receptor subfamily 3, group C, member 1 [NR3C1]) and FK506 binding protein 51 gene (FKBP5), after childhood adversity and associations with risk for psychiatric disorders. Implications for the development of interventions and future research are discussed. En ligne : http://dx.doi.org/10.1017/s0954579416000870 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294

Childhood maltreatment and methylation of FK506 binding protein 5 gene (FKBP5) / Audrey R. TYRKA in Development and Psychopathology, 27-4 (Part 2) (November 2015)  

Public ISBD [article]  inDevelopment and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1637-1645 Titre : Childhood maltreatment and methylation of FK506 binding protein 5 gene (FKBP5) Type de document : Texte imprimé et/ou numérique Auteurs : Audrey R. TYRKA, Auteur ; Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur ; Alison PAQUETTE, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur Article en page(s) : p.1637-1645 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : A growing body of evidence suggests that alterations of the stress response system may be a mechanism by which childhood maltreatment alters risk for psychopathology. FK506 binding protein 51 (FKBP5) binds to the glucocorticoid receptor and alters its ability to respond to stress signaling. The aim of the present study was to examine methylation of the FKBP5 gene (FKBP5), and the role of an FKBP5 genetic variant, in relation to childhood maltreatment in a sample of impoverished preschool-aged children. One hundred seventy-four families participated in this study, including 69 with child welfare documentation of moderate to severe maltreatment in the past 6 months. The children, who ranged in age from 3 to 5 years, were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors; and a composite variable assessed the number exposures to these adversities. Methylation of two sites in intron 7 of FKBP5 was measured via sodium bisulfite pyrosequencing. Maltreated children had significantly lower levels of methylation at both CpG sites (p < .05). Lifetime contextual stress exposure showed a trend for lower levels of methylation at one of the sites, and a trend for an interaction with the FKBP5 polymorphism. A composite adversity variable was associated with lower levels of methylation at one of the sites as well (p < .05). FKBP5 alters glucocorticoid receptor responsiveness, and FKBP5 gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children. En ligne : http://dx.doi.org/10.1017/S0954579415000991 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273 [article] Childhood maltreatment and methylation of FK506 binding protein 5 gene (FKBP5) [Texte imprimé et/ou numérique] / Audrey R. TYRKA, Auteur ; Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur ; Alison PAQUETTE, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur . - p.1637-1645. Langues : Anglais (eng) in Development and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1637-1645 Index. décimale : PER Périodiques Résumé : A growing body of evidence suggests that alterations of the stress response system may be a mechanism by which childhood maltreatment alters risk for psychopathology. FK506 binding protein 51 (FKBP5) binds to the glucocorticoid receptor and alters its ability to respond to stress signaling. The aim of the present study was to examine methylation of the FKBP5 gene (FKBP5), and the role of an FKBP5 genetic variant, in relation to childhood maltreatment in a sample of impoverished preschool-aged children. One hundred seventy-four families participated in this study, including 69 with child welfare documentation of moderate to severe maltreatment in the past 6 months. The children, who ranged in age from 3 to 5 years, were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors; and a composite variable assessed the number exposures to these adversities. Methylation of two sites in intron 7 of FKBP5 was measured via sodium bisulfite pyrosequencing. Maltreated children had significantly lower levels of methylation at both CpG sites (p < .05). Lifetime contextual stress exposure showed a trend for lower levels of methylation at one of the sites, and a trend for an interaction with the FKBP5 polymorphism. A composite adversity variable was associated with lower levels of methylation at one of the sites as well (p < .05). FKBP5 alters glucocorticoid receptor responsiveness, and FKBP5 gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children. En ligne : http://dx.doi.org/10.1017/S0954579415000991 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273

Dynamic stress-related epigenetic regulation of the glucocorticoid receptor gene promoter during early development: The role of child maltreatment / Justin PARENT in Development and Psychopathology, 29-5 (December 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1635-1648 Titre : Dynamic stress-related epigenetic regulation of the glucocorticoid receptor gene promoter during early development: The role of child maltreatment Type de document : Texte imprimé et/ou numérique Auteurs : Justin PARENT, Auteur ; Stephanie H. PARADE, Auteur ; Laura E. LAUMANN, Auteur ; Kathryn K. RIDOUT, Auteur ; Bao-Zhu YANG, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur ; Audrey R. TYRKA, Auteur Article en page(s) : p.1635-1648 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Epigenetics processes may play a vital role in the biological embedding of early environmental adversity and the development of psychopathology. Accumulating evidence suggests that maltreatment is linked to methylation of the glucocorticoid receptor gene, nuclear receptor subfamily 3, group C, member 1 (NR3C1), which is a key regulator of the hypothalamus–pituitary–adrenal axis. However, prior work has been exclusively cross-sectional, greatly constraining our understanding of stress-related epigenetic processes over time. In the current study, we examined the effect of maltreatment and other adversity on change in NR3C1 methylation among at-risk preschoolers to begin to characterize within-child epigenetic changes during this sensitive developmental period. Participants were 260 preschoolers (3–5 years old, 53.8% female), including 51.5% with moderate to severe maltreatment in the past 6 months. Child protection records, semistructured interviews, and parent reports were used to assess child stress exposure. Methylation of exons 1D and 1F of NR3C1 via saliva DNA were measured at two time points approximately 6 months apart. Results indicate that maltreated children evidence higher baseline levels of NR3C1 methylation, significant decreases in methylation over time, and then at follow-up, lower levels of methylation, relative to nonmaltreated preschoolers. Findings from the current study highlight the complex nature of stress-related epigenetic processes during early development. En ligne : http://dx.doi.org/10.1017/S0954579417001298 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323 [article] Dynamic stress-related epigenetic regulation of the glucocorticoid receptor gene promoter during early development: The role of child maltreatment [Texte imprimé et/ou numérique] / Justin PARENT, Auteur ; Stephanie H. PARADE, Auteur ; Laura E. LAUMANN, Auteur ; Kathryn K. RIDOUT, Auteur ; Bao-Zhu YANG, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur ; Audrey R. TYRKA, Auteur . - p.1635-1648. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1635-1648 Index. décimale : PER Périodiques Résumé : Epigenetics processes may play a vital role in the biological embedding of early environmental adversity and the development of psychopathology. Accumulating evidence suggests that maltreatment is linked to methylation of the glucocorticoid receptor gene, nuclear receptor subfamily 3, group C, member 1 (NR3C1), which is a key regulator of the hypothalamus–pituitary–adrenal axis. However, prior work has been exclusively cross-sectional, greatly constraining our understanding of stress-related epigenetic processes over time. In the current study, we examined the effect of maltreatment and other adversity on change in NR3C1 methylation among at-risk preschoolers to begin to characterize within-child epigenetic changes during this sensitive developmental period. Participants were 260 preschoolers (3–5 years old, 53.8% female), including 51.5% with moderate to severe maltreatment in the past 6 months. Child protection records, semistructured interviews, and parent reports were used to assess child stress exposure. Methylation of exons 1D and 1F of NR3C1 via saliva DNA were measured at two time points approximately 6 months apart. Results indicate that maltreated children evidence higher baseline levels of NR3C1 methylation, significant decreases in methylation over time, and then at follow-up, lower levels of methylation, relative to nonmaltreated preschoolers. Findings from the current study highlight the complex nature of stress-related epigenetic processes during early development. En ligne : http://dx.doi.org/10.1017/S0954579417001298 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323

Interleukin 1B gene (IL1B) variation and internalizing symptoms in maltreated preschoolers / Kathryn K. RIDOUT in Development and Psychopathology, 26-4 (Part 2) (November 2014)  

Public ISBD [article]  inDevelopment and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1277-1287 Titre : Interleukin 1B gene (IL1B) variation and internalizing symptoms in maltreated preschoolers Type de document : Texte imprimé et/ou numérique Auteurs : Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur ; Ronald SEIFER, Auteur ; Lawrence H. PRICE, Auteur ; Joel GELERNTER, Auteur ; Paloma FELIZ, Auteur ; Audrey R. TYRKA, Auteur Année de publication : 2014 Article en page(s) : p.1277-1287 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Evidence now implicates inflammatory proteins in the neurobiology of internalizing disorders. Genetic factors may influence individual responses to maltreatment; however, little work has examined inflammatory genetic variants in adults and none in children. The present study examined the role of an interleukin 1B gene (IL1B) variant in preschoolers exposed to maltreatment and other forms of adversity in internalizing symptom development. One hundred ninety-eight families were enrolled, with one child (age 3–5 years) from each family. Adversity measures included child protective service documentation of moderate–severe maltreatment in the last 6 months and interview-assessed contextual stressors. Internalizing symptoms were measured using the Child Behavior Checklist and the Diagnostic Infant and Preschool Assessment. Maltreated children had higher major depressive disorder (MDD) and posttraumatic stress disorder symptoms and marginally higher internalizing symptoms on the Child Behavior Checklist. Controlling for age, sex, and race, IL1B genotype was associated with MDD symptoms (p = .002). Contextual stressors were significantly associated with MDD and posttraumatic stress disorder and marginally with internalizing symptoms. The IL1B genotype interacted with contextual stress such that children homozygous for the minor allele had more MDD symptoms (p = .045). These results suggest that genetic variants of IL1B may modulate the development of internalizing symptoms in the face of childhood adversity. En ligne : http://dx.doi.org/10.1017/S0954579414001023 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245 [article] Interleukin 1B gene (IL1B) variation and internalizing symptoms in maltreated preschoolers [Texte imprimé et/ou numérique] / Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur ; Ronald SEIFER, Auteur ; Lawrence H. PRICE, Auteur ; Joel GELERNTER, Auteur ; Paloma FELIZ, Auteur ; Audrey R. TYRKA, Auteur . - 2014 . - p.1277-1287. Langues : Anglais (eng) in Development and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1277-1287 Index. décimale : PER Périodiques Résumé : Evidence now implicates inflammatory proteins in the neurobiology of internalizing disorders. Genetic factors may influence individual responses to maltreatment; however, little work has examined inflammatory genetic variants in adults and none in children. The present study examined the role of an interleukin 1B gene (IL1B) variant in preschoolers exposed to maltreatment and other forms of adversity in internalizing symptom development. One hundred ninety-eight families were enrolled, with one child (age 3–5 years) from each family. Adversity measures included child protective service documentation of moderate–severe maltreatment in the last 6 months and interview-assessed contextual stressors. Internalizing symptoms were measured using the Child Behavior Checklist and the Diagnostic Infant and Preschool Assessment. Maltreated children had higher major depressive disorder (MDD) and posttraumatic stress disorder symptoms and marginally higher internalizing symptoms on the Child Behavior Checklist. Controlling for age, sex, and race, IL1B genotype was associated with MDD symptoms (p = .002). Contextual stressors were significantly associated with MDD and posttraumatic stress disorder and marginally with internalizing symptoms. The IL1B genotype interacted with contextual stress such that children homozygous for the minor allele had more MDD symptoms (p = .045). These results suggest that genetic variants of IL1B may modulate the development of internalizing symptoms in the face of childhood adversity. En ligne : http://dx.doi.org/10.1017/S0954579414001023 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245

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