Change in FK506 binding protein 5 (FKBP5) methylation over time among preschoolers with adversity / Stephanie H. PARADE in Development and Psychopathology, 29-5 (December 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1627-1634 Titre : Change in FK506 binding protein 5 (FKBP5) methylation over time among preschoolers with adversity Type de document : Texte imprimé et/ou numérique Auteurs : Stephanie H. PARADE, Auteur ; Justin PARENT, Auteur ; Kantoniony RABEMANANJARA, Auteur ; Ronald SEIFER, Auteur ; Carmen J. MARSIT, Auteur ; Bao-Zhu YANG, Auteur ; Huiping ZHANG, Auteur ; Audrey R. TYRKA, Auteur Article en page(s) : p.1627-1634 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : FK506 binding protein 5 (FKBP5) alters stress response system functioning, and childhood maltreatment is associated with methylation of the FKBP5 gene. Yet it is unknown if maltreatment contributes to change in FKBP5 methylation over time. The current study draws upon a sample of 231 preschoolers, including 123 with child welfare documentation of moderate to severe maltreatment in the past 6 months, to understand if maltreatment contributes to change in FKBP5 methylation over a 6-month period. Review of child protection records and semistructured interviews in the home were used to assess maltreatment and exposure to other contextual stressors, as well as service utilization. Methylation of FKBP5 at two CpG sites in intron 7 was measured from saliva DNA at the time of initial study enrollment, and 6 months following enrollment. Child maltreatment was associated with change in FKBP5 methylation over time, but only when children were exposed to high levels of other contextual stressors. Service utilization was associated with increases in methylation over time, but only among children with the FKPB5 rs1360780 protective CC genotype. Methylation of FKBP5 is sensitive to stress exposure and may be a mechanism linking early adversity to long-term health and developmental outcomes. En ligne : http://dx.doi.org/10.1017/S0954579417001286 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323 [article] Change in FK506 binding protein 5 (FKBP5) methylation over time among preschoolers with adversity [Texte imprimé et/ou numérique] / Stephanie H. PARADE, Auteur ; Justin PARENT, Auteur ; Kantoniony RABEMANANJARA, Auteur ; Ronald SEIFER, Auteur ; Carmen J. MARSIT, Auteur ; Bao-Zhu YANG, Auteur ; Huiping ZHANG, Auteur ; Audrey R. TYRKA, Auteur . - p.1627-1634. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1627-1634 Index. décimale : PER Périodiques Résumé : FK506 binding protein 5 (FKBP5) alters stress response system functioning, and childhood maltreatment is associated with methylation of the FKBP5 gene. Yet it is unknown if maltreatment contributes to change in FKBP5 methylation over time. The current study draws upon a sample of 231 preschoolers, including 123 with child welfare documentation of moderate to severe maltreatment in the past 6 months, to understand if maltreatment contributes to change in FKBP5 methylation over a 6-month period. Review of child protection records and semistructured interviews in the home were used to assess maltreatment and exposure to other contextual stressors, as well as service utilization. Methylation of FKBP5 at two CpG sites in intron 7 was measured from saliva DNA at the time of initial study enrollment, and 6 months following enrollment. Child maltreatment was associated with change in FKBP5 methylation over time, but only when children were exposed to high levels of other contextual stressors. Service utilization was associated with increases in methylation over time, but only among children with the FKPB5 rs1360780 protective CC genotype. Methylation of FKBP5 is sensitive to stress exposure and may be a mechanism linking early adversity to long-term health and developmental outcomes. En ligne : http://dx.doi.org/10.1017/S0954579417001286 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323

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

Stress exposure and psychopathology alter methylation of the serotonin receptor 2A (HTR2A) gene in preschoolers / Stephanie H. PARADE in Development and Psychopathology, 29-5 (December 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1619-1626 Titre : Stress exposure and psychopathology alter methylation of the serotonin receptor 2A (HTR2A) gene in preschoolers Type de document : Texte imprimé et/ou numérique Auteurs : Stephanie H. PARADE, Auteur ; Andrew M. NOVICK, Auteur ; Justin PARENT, Auteur ; Ronald SEIFER, Auteur ; Samantha J. KLAVER, Auteur ; Carmen J. MARSIT, Auteur ; Asi Polly GOBIN, Auteur ; Bao-Zhu YANG, Auteur ; Audrey R. TYRKA, Auteur Article en page(s) : p.1619-1626 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Serotonin signaling pathways play a key role in brain development, stress reactivity, and mental health. Epigenetic alterations in the serotonin system may underlie the effect of early life stress on psychopathology. The current study examined methylation of the serotonin receptor 2A (HTR2A) gene in a sample of 228 children including 119 with child welfare documentation of moderate to severe maltreatment within the last 6 months. Child protection records, semistructured interviews in the home, and parent reports were used to assess child stress exposure, psychiatric symptoms, and behavior. The HTR2A genotype and methylation of HTR2A were measured at two CpG sites (–1420 and –1224) from saliva DNA. HTR2A genotype was associated with HTR2A methylation at both CpG sites. HTR2A genotype also moderated associations of contextual stress exposure and HTR2A methylation at site –1420. Contextual stress was positively associated with –1420 methylation among A homozygotes, but negatively associated with –1420 methylation among G homozygotes. Posttraumatic stress disorder and major depressive disorder symptoms were negatively associated with methylation at –1420, but positively associated with methylation at –1224. Results support the view that the serotonin system is sensitive to stress exposure and psychopathology, and HTR2A methylation may be a mechanism by which early adversity is biologically encoded. En ligne : http://dx.doi.org/10.1017/S0954579417001274 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323 [article] Stress exposure and psychopathology alter methylation of the serotonin receptor 2A (HTR2A) gene in preschoolers [Texte imprimé et/ou numérique] / Stephanie H. PARADE, Auteur ; Andrew M. NOVICK, Auteur ; Justin PARENT, Auteur ; Ronald SEIFER, Auteur ; Samantha J. KLAVER, Auteur ; Carmen J. MARSIT, Auteur ; Asi Polly GOBIN, Auteur ; Bao-Zhu YANG, Auteur ; Audrey R. TYRKA, Auteur . - p.1619-1626. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1619-1626 Index. décimale : PER Périodiques Résumé : Serotonin signaling pathways play a key role in brain development, stress reactivity, and mental health. Epigenetic alterations in the serotonin system may underlie the effect of early life stress on psychopathology. The current study examined methylation of the serotonin receptor 2A (HTR2A) gene in a sample of 228 children including 119 with child welfare documentation of moderate to severe maltreatment within the last 6 months. Child protection records, semistructured interviews in the home, and parent reports were used to assess child stress exposure, psychiatric symptoms, and behavior. The HTR2A genotype and methylation of HTR2A were measured at two CpG sites (–1420 and –1224) from saliva DNA. HTR2A genotype was associated with HTR2A methylation at both CpG sites. HTR2A genotype also moderated associations of contextual stress exposure and HTR2A methylation at site –1420. Contextual stress was positively associated with –1420 methylation among A homozygotes, but negatively associated with –1420 methylation among G homozygotes. Posttraumatic stress disorder and major depressive disorder symptoms were negatively associated with methylation at –1420, but positively associated with methylation at –1224. Results support the view that the serotonin system is sensitive to stress exposure and psychopathology, and HTR2A methylation may be a mechanism by which early adversity is biologically encoded. En ligne : http://dx.doi.org/10.1017/S0954579417001274 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323

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