Early adversities accelerate epigenetic aging into adulthood: a 10-year, within-subject analysis / William E. COPELAND in Journal of Child Psychology and Psychiatry, 63-11 (November 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1308-1315 Titre : Early adversities accelerate epigenetic aging into adulthood: a 10-year, within-subject analysis Type de document : Texte imprimé et/ou numérique Auteurs : William E. COPELAND, Auteur ; Lilly SHANAHAN, Auteur ; Ellen W. MCGINNIS, Auteur ; Karolina A. ABERG, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur Article en page(s) : p.1308-1315 Langues : Anglais (eng) Mots-clés : Adolescent  Humans  Child  Young Adult  Adult  Cross-Sectional Studies  Risk Factors  Anxiety Disorders  Aging/genetics  Epigenesis, Genetic  Childhood  DNA methylation  adversity  aging  epigenetic  longitudinal Index. décimale : PER Périodiques Résumé : BACKGROUND: Longitudinal studies are needed to clarify whether early adversities are associated with advanced methylation age or if they actually accelerate methylation aging. This study test whether different dimensions of childhood adversity accelerate biological aging from childhood to adulthood, and, if so, via which mechanisms. METHODS: 381 participants provided one blood sample in childhood (average age 15.0; SD=2.3) and another in young adulthood (average age 23.1; SD=2.8). Participants and their parents provided a median of 6 childhood assessments (total=1,950 childhood observations), reporting exposures to different types of adversity dimensions (i.e. threat, material deprivation, loss, unpredictability). The blood samples were assayed to estimate DNA methylation age in both childhood and adulthood and also change in methylation age across this period. RESULTS: Cross-sectional associations between the childhood adversity dimensions and childhood measures of methylation age were non-significant. In contrast, multiple adversity dimensions were associated with accelerated within-person change in methylation age from adolescence to young adulthood. These associations attenuated in model testing all dimensions at the same time. Accelerated aging increased with increasing number of childhood adversities: Individuals with highest number of adversities experienced 2+ additional years of methylation aging compared to those with no exposure to childhood adversities. The association between total childhood adversity exposure and accelerated aging was partially explained by childhood depressive symptoms, but not anxiety or behavioral symptoms. CONCLUSIONS: Early adversities accelerate epigenetic aging long after they occur, in proportion to the total number of such experiences, and in a manner consistent with a shared effect that crosses multiple early dimensions of risk. En ligne : http://dx.doi.org/10.1111/jcpp.13575 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 [article] Early adversities accelerate epigenetic aging into adulthood: a 10-year, within-subject analysis [Texte imprimé et/ou numérique] / William E. COPELAND, Auteur ; Lilly SHANAHAN, Auteur ; Ellen W. MCGINNIS, Auteur ; Karolina A. ABERG, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur . - p.1308-1315. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1308-1315 Mots-clés : Adolescent  Humans  Child  Young Adult  Adult  Cross-Sectional Studies  Risk Factors  Anxiety Disorders  Aging/genetics  Epigenesis, Genetic  Childhood  DNA methylation  adversity  aging  epigenetic  longitudinal Index. décimale : PER Périodiques Résumé : BACKGROUND: Longitudinal studies are needed to clarify whether early adversities are associated with advanced methylation age or if they actually accelerate methylation aging. This study test whether different dimensions of childhood adversity accelerate biological aging from childhood to adulthood, and, if so, via which mechanisms. METHODS: 381 participants provided one blood sample in childhood (average age 15.0; SD=2.3) and another in young adulthood (average age 23.1; SD=2.8). Participants and their parents provided a median of 6 childhood assessments (total=1,950 childhood observations), reporting exposures to different types of adversity dimensions (i.e. threat, material deprivation, loss, unpredictability). The blood samples were assayed to estimate DNA methylation age in both childhood and adulthood and also change in methylation age across this period. RESULTS: Cross-sectional associations between the childhood adversity dimensions and childhood measures of methylation age were non-significant. In contrast, multiple adversity dimensions were associated with accelerated within-person change in methylation age from adolescence to young adulthood. These associations attenuated in model testing all dimensions at the same time. Accelerated aging increased with increasing number of childhood adversities: Individuals with highest number of adversities experienced 2+ additional years of methylation aging compared to those with no exposure to childhood adversities. The association between total childhood adversity exposure and accelerated aging was partially explained by childhood depressive symptoms, but not anxiety or behavioral symptoms. CONCLUSIONS: Early adversities accelerate epigenetic aging long after they occur, in proportion to the total number of such experiences, and in a manner consistent with a shared effect that crosses multiple early dimensions of risk. En ligne : http://dx.doi.org/10.1111/jcpp.13575 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490

A methylation study implicates the rewiring of brain neural circuits during puberty in the emergence of sex differences in depression symptoms / Robin F. CHAN in Journal of Child Psychology and Psychiatry, 63-7 (July 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-7 (July 2022) . - p.802-809 Titre : A methylation study implicates the rewiring of brain neural circuits during puberty in the emergence of sex differences in depression symptoms Type de document : Texte imprimé et/ou numérique Auteurs : Robin F. CHAN, Auteur ; William E. COPELAND, Auteur ; Min ZHAO, Auteur ; Lin Y. XIE, Auteur ; Jane COSTELLO, Auteur ; Karolina A. ABERG, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur Article en page(s) : p.802-809 Langues : Anglais (eng) Mots-clés : Brain  DNA Methylation  Depression/genetics  Female  Genome-Wide Association Study  Humans  Male  Puberty  Sex Characteristics  Affective disorders  biomarkers  epigenetics  sex differences Index. décimale : PER Périodiques Résumé : BACKGROUND: Women are 1.5-3 times more likely to suffer from depression than men. This sex bias first emerges during puberty and then persists across the reproductive years. As the cause remains largely elusive, we performed a methylation-wide association study (MWAS) to generate novel hypotheses. METHODS: We assayed nearly all 28 million possible methylation sites in blood in 595 blood samples from 487 participants aged 9-17. MWASs were performed to identify methylation sites associated with increasing sex differences in depression symptoms as a function of pubertal stage. Epigenetic deconvolution was applied to perform analyses on a cell-type specific level. RESULTS: In monocytes, a substantial number of significant associations were detected after controlling the FDR at 0.05. These results could not be explained by plasma testosterone/estradiol or current/lifetime trauma. Our top results in monocytes were significantly enriched (ratio of 2.48) for genes in the top of a large genome-wide association study (GWAS) meta-analysis of depression and neurodevelopment-related Gene Ontology (GO) terms that remained significant after correcting for multiple testing. Focusing on our most robust findings (70 genes overlapping with the GWAS meta-analysis and the significant GO terms), we find genes coding for members of each of the major classes of axon guidance molecules (netrins, slits, semaphorins, ephrins, and cell adhesion molecules). Many of these genes were previously implicated in rodent studies of brain development and depression-like phenotypes, as well as human methylation, gene expression and GWAS studies. CONCLUSIONS: Our study suggests that the emergence of sex differences in depression may be related to the differential rewiring of brain circuits between boys and girls during puberty. En ligne : http://dx.doi.org/10.1111/jcpp.13522 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=477 [article] A methylation study implicates the rewiring of brain neural circuits during puberty in the emergence of sex differences in depression symptoms [Texte imprimé et/ou numérique] / Robin F. CHAN, Auteur ; William E. COPELAND, Auteur ; Min ZHAO, Auteur ; Lin Y. XIE, Auteur ; Jane COSTELLO, Auteur ; Karolina A. ABERG, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur . - p.802-809. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-7 (July 2022) . - p.802-809 Mots-clés : Brain  DNA Methylation  Depression/genetics  Female  Genome-Wide Association Study  Humans  Male  Puberty  Sex Characteristics  Affective disorders  biomarkers  epigenetics  sex differences Index. décimale : PER Périodiques Résumé : BACKGROUND: Women are 1.5-3 times more likely to suffer from depression than men. This sex bias first emerges during puberty and then persists across the reproductive years. As the cause remains largely elusive, we performed a methylation-wide association study (MWAS) to generate novel hypotheses. METHODS: We assayed nearly all 28 million possible methylation sites in blood in 595 blood samples from 487 participants aged 9-17. MWASs were performed to identify methylation sites associated with increasing sex differences in depression symptoms as a function of pubertal stage. Epigenetic deconvolution was applied to perform analyses on a cell-type specific level. RESULTS: In monocytes, a substantial number of significant associations were detected after controlling the FDR at 0.05. These results could not be explained by plasma testosterone/estradiol or current/lifetime trauma. Our top results in monocytes were significantly enriched (ratio of 2.48) for genes in the top of a large genome-wide association study (GWAS) meta-analysis of depression and neurodevelopment-related Gene Ontology (GO) terms that remained significant after correcting for multiple testing. Focusing on our most robust findings (70 genes overlapping with the GWAS meta-analysis and the significant GO terms), we find genes coding for members of each of the major classes of axon guidance molecules (netrins, slits, semaphorins, ephrins, and cell adhesion molecules). Many of these genes were previously implicated in rodent studies of brain development and depression-like phenotypes, as well as human methylation, gene expression and GWAS studies. CONCLUSIONS: Our study suggests that the emergence of sex differences in depression may be related to the differential rewiring of brain circuits between boys and girls during puberty. En ligne : http://dx.doi.org/10.1111/jcpp.13522 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=477

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