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Updated: Sep 19, 2025

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Epigenetic Aging in Pediatric-Onset Multiple Sclerosis.

Christopher Goyne1, Ashley E Fair1, Defne Yilmaz2

  • 1Department of Neurosciences, University of California San Diego, CA.

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Summary
This summary is machine-generated.

Pediatric-onset multiple sclerosis (MS) is linked to accelerated biological aging, as measured by epigenetic clocks. This suggests MS may drive premature aging even in young individuals.

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Area of Science:

  • Epigenetics
  • Pediatric Neurology
  • Immunology

Background:

  • Older age in multiple sclerosis (MS) correlates with reduced relapse rates and increased disease progression.
  • Biological age, assessed via epigenetic markers, may offer a more precise measure of aging effects than chronological age.
  • MS-related accelerated aging is a potential factor, distinct from normal aging and comorbidities.

Purpose of the Study:

  • To compare epigenetic age between children with pediatric-onset MS (POMS) and age-matched healthy controls.
  • To investigate if MS contributes to premature aging in pediatric populations.
  • To validate findings in a young cohort, supporting hypotheses from adult MS studies.

Main Methods:

  • A multicenter case-control study analyzed DNA methylation data from whole blood samples.
  • Four established epigenetic clock algorithms were used to calculate epigenetic age.
  • Multivariate regression analysis, adjusted for covariates, compared epigenetic age and age acceleration residual (AAR) between POMS cases and controls.

Main Results:

  • Participants with POMS exhibited greater epigenetic age and AAR compared to controls.
  • This difference was statistically significant for the Hannum and PhenoAge epigenetic clocks.
  • Adjustments were made for age, sex, BMI, tobacco exposure, and socioeconomic status.

Conclusions:

  • Epigenetic age was consistently higher in children with POMS across all tested clocks.
  • The Hannum and PhenoAge clocks showed statistically significant differences, indicating accelerated aging in POMS.
  • These findings suggest that accelerated aging may occur early in the course of MS, even in pediatric patients.