New findings from a study presented at the 2024 ACTRIMS Forum revealed an increase in epigenetic age acceleration among a subgroup of patients with multiple sclerosis.
New interim findings from an ongoing study presented at the 2024
In this study, investigators obtained data from 95 participants (relapsing remitting MS, n = 30; secondary progressive MS, n = 29; primary progressive MS, n = 10; controls, n = 27). Among these groups, EAA was highest in patients with secondary progressive MS using the Horvath (mean = 6.1 [SD, 8.8]), Hannum (mean = 8.3[SD, 10.8]), GrimAge (mean = 2.3[SD, 4.9]), and PhenoAge (mean = 8.9 [SD, 12.9]) clocks. Notably, authors observed no expressive differences in EAA for patients with MS who were treated with anti-CD20 therapy compared with other disease-modifying therapies or no treatment.
Presented by lead author Yinan Zhang, MD, assistant professor of neurology at
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All told, p16INK4a expression demonstrated moderate positive correlation with chronological age among the control group (r = 0.44) but not in the groups of patients with MS (r = 0.05). Similarly, investigators observed positive correlations between p16INK4a and different epigenetic clock measurements of EAA in controls compared in MS. Thus, authors noted that because of the lack of anticipated association between p16INK4a and chronological age in MS, more research is needed to determine the correlations between aging biomarkers and MS disease outcomes.1
In a prior study using DNA methylation-based epigenetic clocks published in Frontiers in Aging Neuroscience, findings showed glial cells of patients with MS had an increased epigenetic age acceleration compared with non-neurological controls, suggesting glial cells of progressive MS exhibit accelerated biological aging.2 Additionally, investigators observed significant sex-specific differences in age acceleration residuals only in neurons using Horvath’s clock. Authors noted that future approaches, such as epigenetic-based therapies, might assist with slowing down or halting age acceleration of the brain of patients with MS because epigenetic changes are reversible by nature.
Conducted by lead author Lara Kular, PhD, assistant professor of clinical neuroscience at Karolinska Institutet, and colleagues, additional findings from that study showed a significant increase in age acceleration residuals, corresponding to 3.6 years, among the glial cells of patients with MS in comparison with the controls (P = .0024) using the Cortical clock, which held following the adjustment for covariates (Padj = 0.0263). Notably, the 4.8-year age acceleration authors observed in MS neurons (P = 0.0054) did not withstand adjustment for covariates and displayed no significant difference in age acceleration residuals in bulk brain tissue between patients with MS and controls.
