Epigenetic aging in Williams syndrome / Satoshi OKAZAKI in Journal of Child Psychology and Psychiatry, 63-12 (December 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-12 (December 2022) . - p.1553-1562 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 [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

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