Telomere length and epigenetic age acceleration in adolescents with anxiety disorders

Abstract Evidence on the relationship between genetics and mental health are flourishing. However, few studies are evaluating early biomarkers that might link genes, environment, and psychopathology. We aimed to study telomere length (TL) and epigenetic age acceleration (AA) in a cohort of adolescen...

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Autores principales: Angelica Cerveira de Baumont, Mauricio Scopel Hoffmann, Andressa Bortoluzzi, Gabriel R. Fries, Patrícia Lavandoski, Lucas K. Grun, Luciano S. P. Guimarães, Fátima T. C. R. Guma, Giovanni Abrahão Salum, Florencia M. Barbé-Tuana, Gisele G. Manfro
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/9b464780231e441eb7f7ca69eb08079a
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spelling oai:doaj.org-article:9b464780231e441eb7f7ca69eb08079a2021-12-02T14:37:39ZTelomere length and epigenetic age acceleration in adolescents with anxiety disorders10.1038/s41598-021-87045-w2045-2322https://doaj.org/article/9b464780231e441eb7f7ca69eb08079a2021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-87045-whttps://doaj.org/toc/2045-2322Abstract Evidence on the relationship between genetics and mental health are flourishing. However, few studies are evaluating early biomarkers that might link genes, environment, and psychopathology. We aimed to study telomere length (TL) and epigenetic age acceleration (AA) in a cohort of adolescents with and without anxiety disorders (N = 234). We evaluated a representative subsample of participants at baseline and after 5 years (n = 76) and categorized them according to their anxiety disorder diagnosis at both time points: (1) control group (no anxiety disorder, n = 18), (2) variable group (anxiety disorder in one evaluation, n = 38), and (3) persistent group (anxiety disorder at both time points, n = 20). We assessed relative mean TL by real-time quantitative PCR and DNA methylation by Infinium HumanMethylation450 BeadChip. We calculated AA using the Horvath age estimation algorithm and analyzed differences among groups using generalized linear mixed models. The persistent group of anxiety disorder did not change TL over time (p = 0.495). The variable group had higher baseline TL (p = 0.003) but no accelerated TL erosion in comparison to the non-anxiety control group (p = 0.053). Furthermore, there were no differences in AA among groups over time. Our findings suggest that adolescents with chronic anxiety did not change telomere length over time, which could be related to a delay in neuronal development in this period of life.Angelica Cerveira de BaumontMauricio Scopel HoffmannAndressa BortoluzziGabriel R. FriesPatrícia LavandoskiLucas K. GrunLuciano S. P. GuimarãesFátima T. C. R. GumaGiovanni Abrahão SalumFlorencia M. Barbé-TuanaGisele G. ManfroNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Angelica Cerveira de Baumont
Mauricio Scopel Hoffmann
Andressa Bortoluzzi
Gabriel R. Fries
Patrícia Lavandoski
Lucas K. Grun
Luciano S. P. Guimarães
Fátima T. C. R. Guma
Giovanni Abrahão Salum
Florencia M. Barbé-Tuana
Gisele G. Manfro
Telomere length and epigenetic age acceleration in adolescents with anxiety disorders
description Abstract Evidence on the relationship between genetics and mental health are flourishing. However, few studies are evaluating early biomarkers that might link genes, environment, and psychopathology. We aimed to study telomere length (TL) and epigenetic age acceleration (AA) in a cohort of adolescents with and without anxiety disorders (N = 234). We evaluated a representative subsample of participants at baseline and after 5 years (n = 76) and categorized them according to their anxiety disorder diagnosis at both time points: (1) control group (no anxiety disorder, n = 18), (2) variable group (anxiety disorder in one evaluation, n = 38), and (3) persistent group (anxiety disorder at both time points, n = 20). We assessed relative mean TL by real-time quantitative PCR and DNA methylation by Infinium HumanMethylation450 BeadChip. We calculated AA using the Horvath age estimation algorithm and analyzed differences among groups using generalized linear mixed models. The persistent group of anxiety disorder did not change TL over time (p = 0.495). The variable group had higher baseline TL (p = 0.003) but no accelerated TL erosion in comparison to the non-anxiety control group (p = 0.053). Furthermore, there were no differences in AA among groups over time. Our findings suggest that adolescents with chronic anxiety did not change telomere length over time, which could be related to a delay in neuronal development in this period of life.
format article
author Angelica Cerveira de Baumont
Mauricio Scopel Hoffmann
Andressa Bortoluzzi
Gabriel R. Fries
Patrícia Lavandoski
Lucas K. Grun
Luciano S. P. Guimarães
Fátima T. C. R. Guma
Giovanni Abrahão Salum
Florencia M. Barbé-Tuana
Gisele G. Manfro
author_facet Angelica Cerveira de Baumont
Mauricio Scopel Hoffmann
Andressa Bortoluzzi
Gabriel R. Fries
Patrícia Lavandoski
Lucas K. Grun
Luciano S. P. Guimarães
Fátima T. C. R. Guma
Giovanni Abrahão Salum
Florencia M. Barbé-Tuana
Gisele G. Manfro
author_sort Angelica Cerveira de Baumont
title Telomere length and epigenetic age acceleration in adolescents with anxiety disorders
title_short Telomere length and epigenetic age acceleration in adolescents with anxiety disorders
title_full Telomere length and epigenetic age acceleration in adolescents with anxiety disorders
title_fullStr Telomere length and epigenetic age acceleration in adolescents with anxiety disorders
title_full_unstemmed Telomere length and epigenetic age acceleration in adolescents with anxiety disorders
title_sort telomere length and epigenetic age acceleration in adolescents with anxiety disorders
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/9b464780231e441eb7f7ca69eb08079a
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