Epigenetic age and telomere length correlations in pediatric-onset multiple sclerosis

Nov 6, 2025Multiple sclerosis (Houndmills, Basingstoke, England)

Links Between Biological Aging and Telomere Length in Children with Multiple Sclerosis

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Abstract

Biological age was analyzed in 270 participants, including 125 with pediatric-onset multiple sclerosis (POMS).

Moderate correlations were observed among different epigenetic clocks used to measure biological age.
No correlations were found between estimates and in the overall participant pool.
In the control group, a modest correlation was identified between telomere length and the PhenoAge clock.
Findings suggest that epigenetic aging markers and telomere length may represent distinct aspects of aging-related biology.

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BACKGROUND: Age is the strongest factor determining disease expression in multiple sclerosis (MS). We previously demonstrated biological age acceleration in pediatric-onset MS (POMS) compared to controls with both epigenetic clocks (DNAm) and (TL). It is unknown whether these markers report overlapping or distinct aging-related processes.

OBJECTIVES: To determine the correlation between DNAm and TL aging markers.

METHODS: We conducted a cross-sectional case-control study within the US Network of Pediatric MS Centers. We calculated age acceleration residuals for the Horvath, Hannum, PhenoAge, and GrimAge epigenetic clocks and measured TL from whole blood samples to estimate telomere to somatic DNA ratios (T/S ratio). We employed multivariable analysis of covariance to assess the correlation between DNAm estimates and TL.

RESULTS: We analyzed biological ages in 270 participants (125 POMS, mean 15.7 years; 145 controls, mean 15.3 years). There were moderate correlations among the different DNAm clocks, but no correlations between DNAm clocks and TL in pooled analyses. In a stratified analysis, only the control group showed a modest correlation between TL and PhenoAge clock ( = 0.2, = 0.06). r p

CONCLUSIONS: DNAm did not correlate with TL in this sample of POMS and controls, suggesting that these biomarkers may capture complementary and non-overlapping elements of aging-related biology.

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Epigenetic age and telomere length correlations in pediatric-onset multiple sclerosis

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