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Case-control meta-analysis of blood DNA methylation and autism spectrum disorder / S. V. ANDREWS in Molecular Autism, 9 (2018)
[article]
Titre : Case-control meta-analysis of blood DNA methylation and autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : S. V. ANDREWS, Auteur ; B. SHEPPARD, Auteur ; G. C. WINDHAM, Auteur ; Laura A. SCHIEVE, Auteur ; Diana SCHENDEL, Auteur ; Lisa A. CROEN, Auteur ; P. CHOPRA, Auteur ; R. S. ALISCH, Auteur ; C. J. NEWSCHAFFER, Auteur ; S. T. WARREN, Auteur ; A. P. FEINBERG, Auteur ; M. D. FALLIN, Auteur ; Christine LADD-ACOSTA, Auteur Article en page(s) : 40p. Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/blood/genetics Case-Control Studies Child, Preschool CpG Islands DNA Methylation Epigenesis, Genetic Female Genome-Wide Association Study Humans Male Autism spectrum disorders Epigenome Peripheral blood Simons Simplex Collection Study to Explore Early Development Index. décimale : PER Périodiques Résumé : Background: Several reports have suggested a role for epigenetic mechanisms in ASD etiology. Epigenome-wide association studies (EWAS) in autism spectrum disorder (ASD) may shed light on particular biological mechanisms. However, studies of ASD cases versus controls have been limited by post-mortem timing and severely small sample sizes. Reports from in-life sampling of blood or saliva have also been very limited in sample size and/or genomic coverage. We present the largest case-control EWAS for ASD to date, combining data from population-based case-control and case-sibling pair studies. Methods: DNA from 968 blood samples from children in the Study to Explore Early Development (SEED 1) was used to generate epigenome-wide array DNA methylation (DNAm) data at 485,512 CpG sites for 453 cases and 515 controls, using the Illumina 450K Beadchip. The Simons Simplex Collection (SSC) provided 450K array DNAm data on an additional 343 cases and their unaffected siblings. We performed EWAS meta-analysis across results from the two data sets, with adjustment for sex and surrogate variables that reflect major sources of biological variation and technical confounding such as cell type, batch, and ancestry. We compared top EWAS results to those from a previous brain-based analysis. We also tested for enrichment of ASD EWAS CpGs for being targets of meQTL associations using available SNP genotype data in the SEED sample. Findings: In this meta-analysis of blood-based DNA from 796 cases and 858 controls, no single CpG met a Bonferroni discovery threshold of p < 1.12 x 10(- 7). Seven CpGs showed differences at p < 1 x 10(- 5) and 48 at 1 x 10(- 4). Of the top 7, 5 showed brain-based ASD associations as well, often with larger effect sizes, and the top 48 overall showed modest concordance (r = 0.31) in direction of effect with cerebellum samples. Finally, we observed suggestive evidence for enrichment of CpG sites controlled by SNPs (meQTL targets) among the EWAS CpG hits, which was consistent across EWAS and meQTL discovery p value thresholds. Conclusions: No single CpG site showed a large enough DNAm difference between cases and controls to achieve epigenome-wide significance in this sample size. However, our results suggest the potential to observe disease associations from blood-based samples. Among the seven sites achieving suggestive statistical significance, we observed consistent, and stronger, effects at the same sites among brain samples. Discovery-oriented EWAS for ASD using blood samples will likely need even larger samples and unified genetic data to further understand DNAm differences in ASD. En ligne : https://dx.doi.org/10.1186/s13229-018-0224-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 40p.[article] Case-control meta-analysis of blood DNA methylation and autism spectrum disorder [Texte imprimé et/ou numérique] / S. V. ANDREWS, Auteur ; B. SHEPPARD, Auteur ; G. C. WINDHAM, Auteur ; Laura A. SCHIEVE, Auteur ; Diana SCHENDEL, Auteur ; Lisa A. CROEN, Auteur ; P. CHOPRA, Auteur ; R. S. ALISCH, Auteur ; C. J. NEWSCHAFFER, Auteur ; S. T. WARREN, Auteur ; A. P. FEINBERG, Auteur ; M. D. FALLIN, Auteur ; Christine LADD-ACOSTA, Auteur . - 40p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 40p.
Mots-clés : Autism Spectrum Disorder/blood/genetics Case-Control Studies Child, Preschool CpG Islands DNA Methylation Epigenesis, Genetic Female Genome-Wide Association Study Humans Male Autism spectrum disorders Epigenome Peripheral blood Simons Simplex Collection Study to Explore Early Development Index. décimale : PER Périodiques Résumé : Background: Several reports have suggested a role for epigenetic mechanisms in ASD etiology. Epigenome-wide association studies (EWAS) in autism spectrum disorder (ASD) may shed light on particular biological mechanisms. However, studies of ASD cases versus controls have been limited by post-mortem timing and severely small sample sizes. Reports from in-life sampling of blood or saliva have also been very limited in sample size and/or genomic coverage. We present the largest case-control EWAS for ASD to date, combining data from population-based case-control and case-sibling pair studies. Methods: DNA from 968 blood samples from children in the Study to Explore Early Development (SEED 1) was used to generate epigenome-wide array DNA methylation (DNAm) data at 485,512 CpG sites for 453 cases and 515 controls, using the Illumina 450K Beadchip. The Simons Simplex Collection (SSC) provided 450K array DNAm data on an additional 343 cases and their unaffected siblings. We performed EWAS meta-analysis across results from the two data sets, with adjustment for sex and surrogate variables that reflect major sources of biological variation and technical confounding such as cell type, batch, and ancestry. We compared top EWAS results to those from a previous brain-based analysis. We also tested for enrichment of ASD EWAS CpGs for being targets of meQTL associations using available SNP genotype data in the SEED sample. Findings: In this meta-analysis of blood-based DNA from 796 cases and 858 controls, no single CpG met a Bonferroni discovery threshold of p < 1.12 x 10(- 7). Seven CpGs showed differences at p < 1 x 10(- 5) and 48 at 1 x 10(- 4). Of the top 7, 5 showed brain-based ASD associations as well, often with larger effect sizes, and the top 48 overall showed modest concordance (r = 0.31) in direction of effect with cerebellum samples. Finally, we observed suggestive evidence for enrichment of CpG sites controlled by SNPs (meQTL targets) among the EWAS CpG hits, which was consistent across EWAS and meQTL discovery p value thresholds. Conclusions: No single CpG site showed a large enough DNAm difference between cases and controls to achieve epigenome-wide significance in this sample size. However, our results suggest the potential to observe disease associations from blood-based samples. Among the seven sites achieving suggestive statistical significance, we observed consistent, and stronger, effects at the same sites among brain samples. Discovery-oriented EWAS for ASD using blood samples will likely need even larger samples and unified genetic data to further understand DNAm differences in ASD. En ligne : https://dx.doi.org/10.1186/s13229-018-0224-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 Epigenetic aging in Williams syndrome / Satoshi OKAZAKI in Journal of Child Psychology and Psychiatry, 63-12 (December 2022)
[article]
Titre : Epigenetic aging in Williams syndrome Type de document : Texte imprimé et/ou numérique Auteurs : Satoshi OKAZAKI, Auteur ; Ryo KIMURA, Auteur ; Ikuo OTSUKA, Auteur ; Kiyotaka TOMIWA, Auteur ; Yasuko FUNABIKI, Auteur ; Masatoshi HAGIWARA, Auteur ; Toshiya MURAI, Auteur ; Akitoyo HISHIMOTO, Auteur Article en page(s) : p.1553-1562 Langues : Anglais (eng) Mots-clés : Humans Williams Syndrome/genetics Aging/genetics DNA Methylation/genetics Biomarkers Epigenesis, Genetic Aging Williams syndrome epigenetics Index. décimale : PER Périodiques Résumé : BACKGROUND: Williams syndrome (WS) is a rare genetic disorder caused by a microdeletion at the 7q11.23 region and is characterized by diverse symptoms encompassing physical and cognitive features. WS was reported to be associated to altered DNA methylation (DNAm) patterns. However, due to the limited information from long-term studies, it remains unclear whether WS accelerates aging. Genome-wide DNAm profiles can serve as "epigenetic clocks" to help estimate biological aging along with age-related markers, such as plasma proteins and telomere length. METHODS: We investigated GrimAge, DNAm-based telomere length (DNAmTL), and other epigenetic clocks in blood samples of 32 patients with WS and 32 healthy controls. RESULTS: We observed a significant acceleration in GrimAge, DNAmTL, and other epigenetic clocks in patients with WS as compared with those of controls. In addition, several GrimAge components, such as adrenomedullin, growth differentiation factor-15, leptin and plasminogen activator inhibitor-1, were altered in patients with WS. CONCLUSIONS: This study provides novel evidence supporting the hypothesis that WS may be associated to accelerated biological aging. A better understanding of the overall underlying biological effects of WS can provide new foundations for improved patient care; thus, long-term follow-up studies are still warranted. En ligne : http://dx.doi.org/10.1111/jcpp.13613 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490
in Journal of Child Psychology and Psychiatry > 63-12 (December 2022) . - p.1553-1562[article] Epigenetic aging in Williams syndrome [Texte imprimé et/ou numérique] / Satoshi OKAZAKI, Auteur ; Ryo KIMURA, Auteur ; Ikuo OTSUKA, Auteur ; Kiyotaka TOMIWA, Auteur ; Yasuko FUNABIKI, Auteur ; Masatoshi HAGIWARA, Auteur ; Toshiya MURAI, Auteur ; Akitoyo HISHIMOTO, Auteur . - p.1553-1562.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-12 (December 2022) . - p.1553-1562
Mots-clés : Humans Williams Syndrome/genetics Aging/genetics DNA Methylation/genetics Biomarkers Epigenesis, Genetic Aging Williams syndrome epigenetics Index. décimale : PER Périodiques Résumé : BACKGROUND: Williams syndrome (WS) is a rare genetic disorder caused by a microdeletion at the 7q11.23 region and is characterized by diverse symptoms encompassing physical and cognitive features. WS was reported to be associated to altered DNA methylation (DNAm) patterns. However, due to the limited information from long-term studies, it remains unclear whether WS accelerates aging. Genome-wide DNAm profiles can serve as "epigenetic clocks" to help estimate biological aging along with age-related markers, such as plasma proteins and telomere length. METHODS: We investigated GrimAge, DNAm-based telomere length (DNAmTL), and other epigenetic clocks in blood samples of 32 patients with WS and 32 healthy controls. RESULTS: We observed a significant acceleration in GrimAge, DNAmTL, and other epigenetic clocks in patients with WS as compared with those of controls. In addition, several GrimAge components, such as adrenomedullin, growth differentiation factor-15, leptin and plasminogen activator inhibitor-1, were altered in patients with WS. CONCLUSIONS: This study provides novel evidence supporting the hypothesis that WS may be associated to accelerated biological aging. A better understanding of the overall underlying biological effects of WS can provide new foundations for improved patient care; thus, long-term follow-up studies are still warranted. En ligne : http://dx.doi.org/10.1111/jcpp.13613 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 Placental methylome analysis from a prospective autism study / D. I. SCHROEDER in Molecular Autism, 7 (2016)
[article]
Titre : Placental methylome analysis from a prospective autism study Type de document : Texte imprimé et/ou numérique Auteurs : D. I. SCHROEDER, Auteur ; Rebecca J. SCHMIDT, Auteur ; F. K. CRARY-DOOLEY, Auteur ; Cheryl K. WALKER, Auteur ; S. OZONOFF, Auteur ; Daniel J. TANCREDI, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; J. M. LASALLE, Auteur Article en page(s) : 51p. Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/diagnosis/genetics Biomarkers/metabolism Child, Preschool DNA Methylation Early Diagnosis Enhancer Elements, Genetic Epigenesis, Genetic Female Genome, Human Genome-Wide Association Study High-Throughput Nucleotide Sequencing Humans Infant, Newborn Intercellular Signaling Peptides and Proteins/genetics/metabolism Male Membrane Proteins/genetics/metabolism Placenta/metabolism Pregnancy Biomarkers DNA methylation Epigenetics Genomics Methylome Placenta Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are increasingly prevalent neurodevelopmental disorders that are behaviorally diagnosed in early childhood. Most ASD cases likely arise from a complex mixture of genetic and environmental factors, an interface where the epigenetic marks of DNA methylation may be useful as risk biomarkers. The placenta is a potentially useful surrogate tissue characterized by a methylation pattern of partially methylated domains (PMDs) and highly methylated domains (HMDs) reflective of methylation patterns observed in the early embryo. METHODS: In this study, we investigated human term placentas from the MARBLES (Markers of Autism Risk in Babies: Learning Early Signs) prospective study by whole genome bisulfite sequencing. We also examined the utility of PMD/HMDs in detecting methylation differences consistent with ASD diagnosis at age three. RESULTS: We found that while human placental methylomes have highly reproducible PMD and HMD locations, there is a greater variation between individuals in methylation levels over PMDs than HMDs due to both sampling and individual variability. In a comparison of methylation differences in placental samples from 24 ASD and 23 typically developing (TD) children, a HMD containing a putative fetal brain enhancer near DLL1 was found to reach genome-wide significance and was validated for significantly higher methylation in ASD by pyrosequencing. CONCLUSIONS: These results suggest that the placenta could be an informative surrogate tissue for predictive ASD biomarkers in high-risk families. En ligne : http://dx.doi.org/10.1186/s13229-016-0114-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329
in Molecular Autism > 7 (2016) . - 51p.[article] Placental methylome analysis from a prospective autism study [Texte imprimé et/ou numérique] / D. I. SCHROEDER, Auteur ; Rebecca J. SCHMIDT, Auteur ; F. K. CRARY-DOOLEY, Auteur ; Cheryl K. WALKER, Auteur ; S. OZONOFF, Auteur ; Daniel J. TANCREDI, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; J. M. LASALLE, Auteur . - 51p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 51p.
Mots-clés : Autism Spectrum Disorder/diagnosis/genetics Biomarkers/metabolism Child, Preschool DNA Methylation Early Diagnosis Enhancer Elements, Genetic Epigenesis, Genetic Female Genome, Human Genome-Wide Association Study High-Throughput Nucleotide Sequencing Humans Infant, Newborn Intercellular Signaling Peptides and Proteins/genetics/metabolism Male Membrane Proteins/genetics/metabolism Placenta/metabolism Pregnancy Biomarkers DNA methylation Epigenetics Genomics Methylome Placenta Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are increasingly prevalent neurodevelopmental disorders that are behaviorally diagnosed in early childhood. Most ASD cases likely arise from a complex mixture of genetic and environmental factors, an interface where the epigenetic marks of DNA methylation may be useful as risk biomarkers. The placenta is a potentially useful surrogate tissue characterized by a methylation pattern of partially methylated domains (PMDs) and highly methylated domains (HMDs) reflective of methylation patterns observed in the early embryo. METHODS: In this study, we investigated human term placentas from the MARBLES (Markers of Autism Risk in Babies: Learning Early Signs) prospective study by whole genome bisulfite sequencing. We also examined the utility of PMD/HMDs in detecting methylation differences consistent with ASD diagnosis at age three. RESULTS: We found that while human placental methylomes have highly reproducible PMD and HMD locations, there is a greater variation between individuals in methylation levels over PMDs than HMDs due to both sampling and individual variability. In a comparison of methylation differences in placental samples from 24 ASD and 23 typically developing (TD) children, a HMD containing a putative fetal brain enhancer near DLL1 was found to reach genome-wide significance and was validated for significantly higher methylation in ASD by pyrosequencing. CONCLUSIONS: These results suggest that the placenta could be an informative surrogate tissue for predictive ASD biomarkers in high-risk families. En ligne : http://dx.doi.org/10.1186/s13229-016-0114-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329 Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children / Ashley Y. SONG in Autism Research, 15-12 (December 2022)
[article]
Titre : Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children Type de document : Texte imprimé et/ou numérique Auteurs : Ashley Y. SONG, Auteur ; Kelly BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Homayoon FARZADEGAN, Auteur ; Kristen LYALL, Auteur ; M Daniele FALLIN, Auteur ; Heather E. VOLK, Auteur ; Christine LADD-ACOSTA, Auteur Article en page(s) : p.2359-2370 Langues : Anglais (eng) Mots-clés : Child Male Pregnancy Female Humans Autism Spectrum Disorder/epidemiology/genetics Prospective Studies Parents Cognition Biological Products Epigenesis, Genetic DNA methylation age acceleration autism spectrum disorder autism-related traits biologic age epigenetic age parental age Index. décimale : PER Périodiques Résumé : Parental age is a known risk factor for autism spectrum disorder (ASD), however, studies to identify the biologic changes underpinning this association are limited. In recent years, "epigenetic clock" algorithms have been developed to estimate biologic age and to evaluate how the epigenetic aging impacts health and disease. In this study, we examined the relationship between parental epigenetic aging and their child's prospective risk of ASD and autism related quantitative traits in the Early Autism Risk Longitudinal Investigation study. Estimates of epigenetic age were computed using three robust clock algorithms and DNA methylation measures from the Infinium HumanMethylation450k platform for maternal blood and paternal blood specimens collected during pregnancy. Epigenetic age acceleration was defined as the residual of regressing chronological age on epigenetic age while accounting for cell type proportions. Multinomial logistic regression and linear regression models were completed adjusting for potential confounders for both maternal epigenetic age acceleration (n = 163) and paternal epigenetic age acceleration (n = 80). We found accelerated epigenetic aging in mothers estimated by Hannum's clock was significantly associated with lower cognitive ability and function in offspring at 12 months, as measured by Mullen Scales of Early Learning scores (Î2 = -1.66, 95% CI: -3.28, -0.04 for a one-unit increase). We also observed a marginal association between accelerated maternal epigenetic aging by Horvath's clock and increased odds of ASD in offspring at 36 months of age (aOR = 1.12, 95% CI: 0.99, 1.26). By contrast, fathers accelerated aging was marginally associated with decreased ASD risk in their offspring (aOR = 0.83, 95% CI: 0.68, 1.01). Our findings suggest epigenetic aging could play a role in parental age risks on child brain development. En ligne : http://dx.doi.org/10.1002/aur.2822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488
in Autism Research > 15-12 (December 2022) . - p.2359-2370[article] Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children [Texte imprimé et/ou numérique] / Ashley Y. SONG, Auteur ; Kelly BAKULSKI, Auteur ; Jason I. FEINBERG, Auteur ; Craig NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Homayoon FARZADEGAN, Auteur ; Kristen LYALL, Auteur ; M Daniele FALLIN, Auteur ; Heather E. VOLK, Auteur ; Christine LADD-ACOSTA, Auteur . - p.2359-2370.
Langues : Anglais (eng)
in Autism Research > 15-12 (December 2022) . - p.2359-2370
Mots-clés : Child Male Pregnancy Female Humans Autism Spectrum Disorder/epidemiology/genetics Prospective Studies Parents Cognition Biological Products Epigenesis, Genetic DNA methylation age acceleration autism spectrum disorder autism-related traits biologic age epigenetic age parental age Index. décimale : PER Périodiques Résumé : Parental age is a known risk factor for autism spectrum disorder (ASD), however, studies to identify the biologic changes underpinning this association are limited. In recent years, "epigenetic clock" algorithms have been developed to estimate biologic age and to evaluate how the epigenetic aging impacts health and disease. In this study, we examined the relationship between parental epigenetic aging and their child's prospective risk of ASD and autism related quantitative traits in the Early Autism Risk Longitudinal Investigation study. Estimates of epigenetic age were computed using three robust clock algorithms and DNA methylation measures from the Infinium HumanMethylation450k platform for maternal blood and paternal blood specimens collected during pregnancy. Epigenetic age acceleration was defined as the residual of regressing chronological age on epigenetic age while accounting for cell type proportions. Multinomial logistic regression and linear regression models were completed adjusting for potential confounders for both maternal epigenetic age acceleration (n = 163) and paternal epigenetic age acceleration (n = 80). We found accelerated epigenetic aging in mothers estimated by Hannum's clock was significantly associated with lower cognitive ability and function in offspring at 12 months, as measured by Mullen Scales of Early Learning scores (Î2 = -1.66, 95% CI: -3.28, -0.04 for a one-unit increase). We also observed a marginal association between accelerated maternal epigenetic aging by Horvath's clock and increased odds of ASD in offspring at 36 months of age (aOR = 1.12, 95% CI: 0.99, 1.26). By contrast, fathers accelerated aging was marginally associated with decreased ASD risk in their offspring (aOR = 0.83, 95% CI: 0.68, 1.01). Our findings suggest epigenetic aging could play a role in parental age risks on child brain development. En ligne : http://dx.doi.org/10.1002/aur.2822 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=488 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)
[article]
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
in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1308-1315[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 Editorial: Accelerated epigenetic ageing as a consequence of early environmental adversity / Barbara FRANKE in Journal of Child Psychology and Psychiatry, 63-11 (November 2022)
PermalinkExaggerated CpH methylation in the autism-affected brain / S. E. ELLIS in Molecular Autism, 8 (2017)
PermalinkIntegrated genome-wide Alu methylation and transcriptome profiling analyses reveal novel epigenetic regulatory networks associated with autism spectrum disorder / T. SAELIW in Molecular Autism, 9 (2018)
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