Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder

Major depressive disorder (MDD) is known to cause significant disability. Genome-wide DNA methylation (DNAm) profiles can be used to estimate biological aging and as epigenetic clocks. However, information on epigenetic clocks reported in MDD patients is inconsistent. Since antidepressants are likel...

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Autores principales: Shindo, Ryota, Tanifuji, Takaki, Okazaki, Satoshi, Otsuka, Ikuo, Shirai, Toshiyuki, Mouri, Kentaro, Horai, Tadasu, Hishimoto, Akitoyo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
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Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10482893/
https://www.ncbi.nlm.nih.gov/pubmed/37673891
http://dx.doi.org/10.1038/s41514-023-00117-1
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author Shindo, Ryota
Tanifuji, Takaki
Okazaki, Satoshi
Otsuka, Ikuo
Shirai, Toshiyuki
Mouri, Kentaro
Horai, Tadasu
Hishimoto, Akitoyo
author_facet Shindo, Ryota
Tanifuji, Takaki
Okazaki, Satoshi
Otsuka, Ikuo
Shirai, Toshiyuki
Mouri, Kentaro
Horai, Tadasu
Hishimoto, Akitoyo
author_sort Shindo, Ryota
collection PubMed
description Major depressive disorder (MDD) is known to cause significant disability. Genome-wide DNA methylation (DNAm) profiles can be used to estimate biological aging and as epigenetic clocks. However, information on epigenetic clocks reported in MDD patients is inconsistent. Since antidepressants are likely confounders, we evaluated biological aging using various DNAm-based predictors in patients with MDD who had never received depression medication. A publicly available dataset consisting of whole blood samples from untreated MDD patients (n = 40) and controls (n = 40) was used. We analyzed five epigenetic clocks (HorvathAge, HannumAge, SkinBloodAge, PhenoAge, and GrimAge), DNAm-based telomere length (DNAmTL), and DNAm-based age-related plasma proteins (GrimAge components), as well as DNAm-based white blood cell composition. The results indicate that patients with untreated MDD were significantly associated with epigenetic aging acceleration in HannumAge and GrimAge. Furthermore, a decrease in natural killer cells, based on DNAm, was observed in patients with untreated MDD.
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spelling pubmed-104828932023-09-08 Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder Shindo, Ryota Tanifuji, Takaki Okazaki, Satoshi Otsuka, Ikuo Shirai, Toshiyuki Mouri, Kentaro Horai, Tadasu Hishimoto, Akitoyo NPJ Aging Article Major depressive disorder (MDD) is known to cause significant disability. Genome-wide DNA methylation (DNAm) profiles can be used to estimate biological aging and as epigenetic clocks. However, information on epigenetic clocks reported in MDD patients is inconsistent. Since antidepressants are likely confounders, we evaluated biological aging using various DNAm-based predictors in patients with MDD who had never received depression medication. A publicly available dataset consisting of whole blood samples from untreated MDD patients (n = 40) and controls (n = 40) was used. We analyzed five epigenetic clocks (HorvathAge, HannumAge, SkinBloodAge, PhenoAge, and GrimAge), DNAm-based telomere length (DNAmTL), and DNAm-based age-related plasma proteins (GrimAge components), as well as DNAm-based white blood cell composition. The results indicate that patients with untreated MDD were significantly associated with epigenetic aging acceleration in HannumAge and GrimAge. Furthermore, a decrease in natural killer cells, based on DNAm, was observed in patients with untreated MDD. Nature Publishing Group UK 2023-09-06 /pmc/articles/PMC10482893/ /pubmed/37673891 http://dx.doi.org/10.1038/s41514-023-00117-1 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Shindo, Ryota
Tanifuji, Takaki
Okazaki, Satoshi
Otsuka, Ikuo
Shirai, Toshiyuki
Mouri, Kentaro
Horai, Tadasu
Hishimoto, Akitoyo
Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder
title Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder
title_full Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder
title_fullStr Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder
title_full_unstemmed Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder
title_short Accelerated epigenetic aging and decreased natural killer cells based on DNA methylation in patients with untreated major depressive disorder
title_sort accelerated epigenetic aging and decreased natural killer cells based on dna methylation in patients with untreated major depressive disorder
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10482893/
https://www.ncbi.nlm.nih.gov/pubmed/37673891
http://dx.doi.org/10.1038/s41514-023-00117-1
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