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Lookup NU author(s): Dr Arthur PrattORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© The Author(s) 2025.Rheumatoid arthritis (RA) is an age-related chronic inflammatory disease which may include accelerated biological ageing processes in its pathogenesis. To determine if increased biological age is associated with risk of RA and/or is present once disease is established. We used DNA methylation to compare biological age (epigenetic age) of immune cells in adults at risk of RA and those with confirmed RA, including twins discordant for RA. The established RA studies were secondary analyses of existing DNA methylation data. Sub-group analysis considered the influence of ethnicity. Four epigenetic clocks were used to determine DNA methylation age. DNA methylation age was no different in adults at risk of RA in the Leiden Clinically Suspect Arthralgia (CSA) cohort (n = 38 developed RA, n = 24 did not), and there was also no difference in DNA methylation age between 77 UK twins discordant for RA, or adults with established RA from the Swedish EIRA cohort (n = 342) compared to healthy controls (n = 328). A sub-group analysis of RA patients of South Asian ethnicity (10 RA patients, 14 healthy controls) showed DNA methylation age acceleration of 3.3 years (p = 0.00014) using the mean DNA methylation age of four epigenetic clocks. Our study suggests that epigenetic age acceleration may be differentially influenced by South Asian ethnicity, but that RA was not generally associated with accelerated epigenetic age. The higher epigenetic age in the South Asian patients may explain the earlier age of onset in this minority ethnic population.
Author(s): Sharma-Oates A, Dunne N, Raza K, Padyukov L, Rivera N, van der Helm-van Mil A, Pratt AG, Duggal NA, Jones SW, Lord JM
Publication type: Article
Publication status: Published
Journal: GeroScience
Year: 2025
Pages: epub ahead of print
Online publication date: 11/01/2025
Acceptance date: 31/12/2024
Date deposited: 25/03/2025
ISSN (print): 2509-2715
ISSN (electronic): 2509-2723
Publisher: Springer Science and Business Media Deutschland GmbH
URL: https://doi.org/10.1007/s11357-025-01508-w
DOI: 10.1007/s11357-025-01508-w
Data Access Statement: The primary data in this study are available upon reasonable request to the corresponding author.
PubMed id: 39797936
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