DNA methylation at birth and lateral ventricular volume in childhood: a neuroimaging epigenetics study / Esther WALTON ; Alexander NEUMANN ; Chris H. L. THIO ; Janine F. FELIX ; Marinus H. VAN IJZENDOORN ; Irene PAPPA ; Charlotte A. M. CECIL in Journal of Child Psychology and Psychiatry, 65-1 (January 2024)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 65-1 (January 2024) . - p.77-90 Titre : DNA methylation at birth and lateral ventricular volume in childhood: a neuroimaging epigenetics study Type de document : Texte imprimé et/ou numérique Auteurs : Esther WALTON, Auteur ; Alexander NEUMANN, Auteur ; Chris H. L. THIO, Auteur ; Janine F. FELIX, Auteur ; Marinus H. VAN IJZENDOORN, Auteur ; Irene PAPPA, Auteur ; Charlotte A. M. CECIL, Auteur Article en page(s) : p.77-90 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background Lateral ventricular volume (LVV) enlargement has been repeatedly linked to schizophrenia; yet, what biological factors shape LVV during early development remain unclear. DNA methylation (DNAm), an essential process for neurodevelopment that is altered in schizophrenia, is a key molecular system of interest. Methods In this study, we conducted the first epigenome-wide association study of neonatal DNAm in cord blood with LVV in childhood (measured using T1-weighted brain scans at 10?years), based on data from a large population-based birth cohort, the Generation R Study (N?=?840). Employing both probe-level and methylation profile score (MPS) approaches, we further examined whether epigenetic modifications identified at birth in cord blood are: (a) also observed cross-sectionally in childhood using peripheral blood DNAm at age of 10?years (Generation R, N?=?370) and (b) prospectively associated with LVV measured in young adulthood in an all-male sample from the Avon Longitudinal Study of Parents and Children (ALSPAC, N?=?114). Results At birth, DNAm levels at four CpGs (annotated to potassium channel tetramerization domain containing 3, KCTD3; SHH signaling and ciliogenesis regulator, SDCCAG8; glutaredoxin, GLRX) prospectively associated with childhood LVV after genome-wide correction; these genes have been implicated in brain development and psychiatric traits including schizophrenia. An MPS capturing a broader epigenetic profile of LVV ? but not individual top hits ? showed significant cross-sectional associations with LVV in childhood in Generation R and prospectively associated with LVV in early adulthood within ALSPAC. Conclusions This study finds suggestive evidence that DNAm at birth prospectively associates with LVV at different life stages, albeit with small effect sizes. The prediction of MPS on LVV in a childhood sample and an independent male adult sample further underscores the stability and reproducibility of DNAm as a potential marker for LVV. Future studies with larger samples and comparable time points across development are needed to further elucidate how DNAm associates with this clinically relevant brain structure and risk for neuropsychiatric disorders, and what factors explain the identified DNAm profile of LVV at birth. En ligne : https://doi.org/10.1111/jcpp.13866 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=518 [article] DNA methylation at birth and lateral ventricular volume in childhood: a neuroimaging epigenetics study [Texte imprimé et/ou numérique] / Esther WALTON, Auteur ; Alexander NEUMANN, Auteur ; Chris H. L. THIO, Auteur ; Janine F. FELIX, Auteur ; Marinus H. VAN IJZENDOORN, Auteur ; Irene PAPPA, Auteur ; Charlotte A. M. CECIL, Auteur . - p.77-90. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 65-1 (January 2024) . - p.77-90 Index. décimale : PER Périodiques Résumé : Background Lateral ventricular volume (LVV) enlargement has been repeatedly linked to schizophrenia; yet, what biological factors shape LVV during early development remain unclear. DNA methylation (DNAm), an essential process for neurodevelopment that is altered in schizophrenia, is a key molecular system of interest. Methods In this study, we conducted the first epigenome-wide association study of neonatal DNAm in cord blood with LVV in childhood (measured using T1-weighted brain scans at 10?years), based on data from a large population-based birth cohort, the Generation R Study (N?=?840). Employing both probe-level and methylation profile score (MPS) approaches, we further examined whether epigenetic modifications identified at birth in cord blood are: (a) also observed cross-sectionally in childhood using peripheral blood DNAm at age of 10?years (Generation R, N?=?370) and (b) prospectively associated with LVV measured in young adulthood in an all-male sample from the Avon Longitudinal Study of Parents and Children (ALSPAC, N?=?114). Results At birth, DNAm levels at four CpGs (annotated to potassium channel tetramerization domain containing 3, KCTD3; SHH signaling and ciliogenesis regulator, SDCCAG8; glutaredoxin, GLRX) prospectively associated with childhood LVV after genome-wide correction; these genes have been implicated in brain development and psychiatric traits including schizophrenia. An MPS capturing a broader epigenetic profile of LVV ? but not individual top hits ? showed significant cross-sectional associations with LVV in childhood in Generation R and prospectively associated with LVV in early adulthood within ALSPAC. Conclusions This study finds suggestive evidence that DNAm at birth prospectively associates with LVV at different life stages, albeit with small effect sizes. The prediction of MPS on LVV in a childhood sample and an independent male adult sample further underscores the stability and reproducibility of DNAm as a potential marker for LVV. Future studies with larger samples and comparable time points across development are needed to further elucidate how DNAm associates with this clinically relevant brain structure and risk for neuropsychiatric disorders, and what factors explain the identified DNAm profile of LVV at birth. En ligne : https://doi.org/10.1111/jcpp.13866 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=518

Methylation matters: FK506 binding protein 51 (FKBP5) methylation moderates the associations of FKBP5 genotype and resistant attachment with stress regulation / Rosa H. MULDER in Development and Psychopathology, 29-2 (May 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-2 (May 2017) . - p.491-503 Titre : Methylation matters: FK506 binding protein 51 (FKBP5) methylation moderates the associations of FKBP5 genotype and resistant attachment with stress regulation Type de document : Texte imprimé et/ou numérique Auteurs : Rosa H. MULDER, Auteur ; Jolien RIJLAARSDAM, Auteur ; Maartje P. C. M. LUIJK, Auteur ; Frank C. VERHULST, Auteur ; Janine F. FELIX, Auteur ; Henning TIEMEIER, Auteur ; Marian J. BAKERMANS-KRANENBURG, Auteur ; Marinus H. VAN IJZENDOORN, Auteur Article en page(s) : p.491-503 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The parent–child attachment relationship plays an important role in the development of the infant's stress regulation system. However, genetic and epigenetic factors such as FK506 binding protein 51 (FKBP5) genotype and DNA methylation have also been associated with hypothalamus–pituitary–adrenal axis functioning. In the current study, we examined how parent–child dyadic regulation works in concert with genetic and epigenetic aspects of stress regulation. We study the associations of attachment, extreme maternal insensitivity, FKBP5 single nucleotide polymorphism 1360780, and FKBP5 methylation, with cortisol reactivity to the Strange Situation Procedure in 298 14-month-old infants. The results indicate that FKBP5 methylation moderates the associations of FKBP5 genotype and resistant attachment with cortisol reactivity. We conclude that the inclusion of epigenetics in the field of developmental psychopathology may lead to a more precise picture of the interplay between genetic makeup and parenting in shaping stress reactivity. En ligne : http://dx.doi.org/10.1017/s095457941700013x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=305 [article] Methylation matters: FK506 binding protein 51 (FKBP5) methylation moderates the associations of FKBP5 genotype and resistant attachment with stress regulation [Texte imprimé et/ou numérique] / Rosa H. MULDER, Auteur ; Jolien RIJLAARSDAM, Auteur ; Maartje P. C. M. LUIJK, Auteur ; Frank C. VERHULST, Auteur ; Janine F. FELIX, Auteur ; Henning TIEMEIER, Auteur ; Marian J. BAKERMANS-KRANENBURG, Auteur ; Marinus H. VAN IJZENDOORN, Auteur . - p.491-503. Langues : Anglais (eng) in Development and Psychopathology > 29-2 (May 2017) . - p.491-503 Index. décimale : PER Périodiques Résumé : The parent–child attachment relationship plays an important role in the development of the infant's stress regulation system. However, genetic and epigenetic factors such as FK506 binding protein 51 (FKBP5) genotype and DNA methylation have also been associated with hypothalamus–pituitary–adrenal axis functioning. In the current study, we examined how parent–child dyadic regulation works in concert with genetic and epigenetic aspects of stress regulation. We study the associations of attachment, extreme maternal insensitivity, FKBP5 single nucleotide polymorphism 1360780, and FKBP5 methylation, with cortisol reactivity to the Strange Situation Procedure in 298 14-month-old infants. The results indicate that FKBP5 methylation moderates the associations of FKBP5 genotype and resistant attachment with cortisol reactivity. We conclude that the inclusion of epigenetics in the field of developmental psychopathology may lead to a more precise picture of the interplay between genetic makeup and parenting in shaping stress reactivity. En ligne : http://dx.doi.org/10.1017/s095457941700013x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=305

Prenatal stress exposure, oxytocin receptor gene (OXTR) methylation, and child autistic traits: The moderating role of OXTR rs53576 genotype / Jolien RIJLAARSDAM in Autism Research, 10-3 (March 2017)  

Public ISBD [article]  inAutism Research > 10-3 (March 2017) . - p.430-438 Titre : Prenatal stress exposure, oxytocin receptor gene (OXTR) methylation, and child autistic traits: The moderating role of OXTR rs53576 genotype Type de document : Texte imprimé et/ou numérique Auteurs : Jolien RIJLAARSDAM, Auteur ; Marinus H. VAN IJZENDOORN, Auteur ; Frank C. VERHULST, Auteur ; Vincent W.V. JADDOE, Auteur ; Janine F. FELIX, Auteur ; Henning TIEMEIER, Auteur ; Marian J. BAKERMANS-KRANENBURG, Auteur Article en page(s) : p.430-438 Langues : Anglais (eng) Mots-clés : DNA methylation  oxytocin receptor gene (OXTR)  autistic traits  stress exposure Index. décimale : PER Périodiques Résumé : Findings of studies investigating OXTR SNP rs53576 (G-A) variation in social behavior have been inconsistent, possibly because DNA methylation after stress exposure was eliminated from consideration. Our goal was to examine OXTR rs53576 allele-specific sensitivity for neonatal OXTR DNA methylation in relation to (1) a prenatal maternal stress composite, and (2) child autistic traits. Prospective data from fetal life to age 6 years were collected in a total of 743 children participating in the Generation R Study. Prenatal maternal stress exposure was uniquely associated with child autistic traits but was unrelated to OXTR methylation across both OXTR rs53576 G-allele homozygous children and A-allele carriers. For child autistic traits in general and social communication problems in particular, we observed a significant OXTR rs53576 genotype by OXTR methylation interaction in the absence of main effects, suggesting that opposing effects cancelled each other out. Indeed, OXTR methylation levels were positively associated with social problems for OXTR rs53576 G-allele homozygous children but not for A-allele carriers. These results highlight the importance of incorporating epi-allelic information and support the role of OXTR methylation in child autistic traits. En ligne : http://dx.doi.org/10.1002/aur.1681 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=304 [article] Prenatal stress exposure, oxytocin receptor gene (OXTR) methylation, and child autistic traits: The moderating role of OXTR rs53576 genotype [Texte imprimé et/ou numérique] / Jolien RIJLAARSDAM, Auteur ; Marinus H. VAN IJZENDOORN, Auteur ; Frank C. VERHULST, Auteur ; Vincent W.V. JADDOE, Auteur ; Janine F. FELIX, Auteur ; Henning TIEMEIER, Auteur ; Marian J. BAKERMANS-KRANENBURG, Auteur . - p.430-438. Langues : Anglais (eng) in Autism Research > 10-3 (March 2017) . - p.430-438 Mots-clés : DNA methylation  oxytocin receptor gene (OXTR)  autistic traits  stress exposure Index. décimale : PER Périodiques Résumé : Findings of studies investigating OXTR SNP rs53576 (G-A) variation in social behavior have been inconsistent, possibly because DNA methylation after stress exposure was eliminated from consideration. Our goal was to examine OXTR rs53576 allele-specific sensitivity for neonatal OXTR DNA methylation in relation to (1) a prenatal maternal stress composite, and (2) child autistic traits. Prospective data from fetal life to age 6 years were collected in a total of 743 children participating in the Generation R Study. Prenatal maternal stress exposure was uniquely associated with child autistic traits but was unrelated to OXTR methylation across both OXTR rs53576 G-allele homozygous children and A-allele carriers. For child autistic traits in general and social communication problems in particular, we observed a significant OXTR rs53576 genotype by OXTR methylation interaction in the absence of main effects, suggesting that opposing effects cancelled each other out. Indeed, OXTR methylation levels were positively associated with social problems for OXTR rs53576 G-allele homozygous children but not for A-allele carriers. These results highlight the importance of incorporating epi-allelic information and support the role of OXTR methylation in child autistic traits. En ligne : http://dx.doi.org/10.1002/aur.1681 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=304

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