Centre d'Information et de documentation du CRA Rhône-Alpes
CRA
Informations pratiques
-
Adresse
Centre d'information et de documentation
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexHoraires
Lundi au Vendredi
9h00-12h00 13h30-16h00Contact
Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Résultat de la recherche
3 recherche sur le mot-clé 'Aging/genetics'
Affiner la recherche Générer le flux rss de la recherche
Partager le résultat de cette recherche Faire une suggestion
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 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 Editorial: Accelerated epigenetic ageing as a consequence of early environmental adversity / Barbara FRANKE in Journal of Child Psychology and Psychiatry, 63-11 (November 2022)
[article]
Titre : Editorial: Accelerated epigenetic ageing as a consequence of early environmental adversity Type de document : Texte imprimé et/ou numérique Auteurs : Barbara FRANKE, Auteur Article en page(s) : p.1219-1221 Langues : Anglais (eng) Mots-clés : Adolescent Humans Epigenesis, Genetic Aging/genetics DNA methylation Great Smoky Mountains Study environmental adversity epigenetic ageing Index. décimale : PER Périodiques Résumé : In this editorial, I discuss findings and implications of a hypothesis-generating study by Copeland and colleagues showing that early adverse events related to unpredictability as well as a cumulative score summarising environmental adversity in childhood and adolescence are linked to accelerated epigenetic ageing. The setting of this study is the longitudinal Great Smoky Mountains Study, a richly phenotyped longitudinal cohort with biological information. In my discussion, I focus on potential mechanisms behind the reported findings and opportunities for next steps, for example provided by the richness of data in the cohort used in this study. En ligne : http://dx.doi.org/10.1111/jcpp.13711 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=489
in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1219-1221[article] Editorial: Accelerated epigenetic ageing as a consequence of early environmental adversity [Texte imprimé et/ou numérique] / Barbara FRANKE, Auteur . - p.1219-1221.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1219-1221
Mots-clés : Adolescent Humans Epigenesis, Genetic Aging/genetics DNA methylation Great Smoky Mountains Study environmental adversity epigenetic ageing Index. décimale : PER Périodiques Résumé : In this editorial, I discuss findings and implications of a hypothesis-generating study by Copeland and colleagues showing that early adverse events related to unpredictability as well as a cumulative score summarising environmental adversity in childhood and adolescence are linked to accelerated epigenetic ageing. The setting of this study is the longitudinal Great Smoky Mountains Study, a richly phenotyped longitudinal cohort with biological information. In my discussion, I focus on potential mechanisms behind the reported findings and opportunities for next steps, for example provided by the richness of data in the cohort used in this study. En ligne : http://dx.doi.org/10.1111/jcpp.13711 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=489