Acta neurologica Belgica · 2026
Shorter Leukocyte telomere length as a marker of biological aging in relapsing-remitting multiple sclerosis.
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Karacan Ilker, Susgun Seda, Savasci Didem, Yigit Begum, Yozlu Deniz, Korkmaz Nur Damla, Duzenli Omer Faruk, Yabaci Aysegul, Yucesan Emrah, Gursoy Azize Esra Basar
Аннотация
BACKGROUND: Multiple sclerosis (MS) is increasingly recognized not only as an immune-mediated demyelinating disease but also as a disorder characterized by accelerated biological aging. Leukocyte telomere length (LTL) serves as a hallmark biomarker of cellular senescence, yet its predictive role in early-stage MS and its modulation by shelterin complex genetics remain to be fully elucidated.
METHODS: In this cross-sectional study, relative LTL was measured via quantitative polymerase chain reaction in a highly characterized, young cohort of patients with relapsing-remitting MS (RRMS; n = 40, age ≤ 40) and age- and sex-matched healthy controls (n = 39). High-resolution melting analysis was utilized to genotype key shelterin complex polymorphisms: TERF1 (rs10107605, rs1545827) and TERF2 (rs251796). Comprehensive genetic association testing across codominant, dominant, recessive, overdominant, and additive models was conducted alongside clinical/imaging phenotype correlations.
RESULTS: LTL was significantly shorter in RRMS patients than in healthy controls (p = 0.005), suggesting evidence of accelerated biological aging even in this relatively young cohort. Receiver operating characteristic analysis demonstrated modest discriminatory performance area under the curve = 0.698 (95% CI: 0.60-0.79). Notably, across all inheritance models, TERF1 and TERF2 polymorphisms exhibited no significant association with LTL. Furthermore, subgroup analyses revealed that LTL attrition was independent of chronological age, sex, smoking status, or disease duration, indicating that telomere erosion is driven primarily by intrinsic disease-related systemic stress rather than host shelterin genetic predisposition.
CONCLUSIONS: Our findings demonstrate that leukocyte telomere shortening represents a distinct molecular signature of premature biological aging in young MS patients. By decoupling telomere depletion from primary shelterin genetic variability, this work consistent with disease-driven immunosenescence in MS. In long-standing, heterogeneous disorders like MS, LTL emerges as a promising biomarker for capturing biological decline prior to irreversible neurodegeneration. This study provides a basis for future longitudinal multi-omics investigations exploring telomere dynamics in chronic neuroinflammation.
METHODS: In this cross-sectional study, relative LTL was measured via quantitative polymerase chain reaction in a highly characterized, young cohort of patients with relapsing-remitting MS (RRMS; n = 40, age ≤ 40) and age- and sex-matched healthy controls (n = 39). High-resolution melting analysis was utilized to genotype key shelterin complex polymorphisms: TERF1 (rs10107605, rs1545827) and TERF2 (rs251796). Comprehensive genetic association testing across codominant, dominant, recessive, overdominant, and additive models was conducted alongside clinical/imaging phenotype correlations.
RESULTS: LTL was significantly shorter in RRMS patients than in healthy controls (p = 0.005), suggesting evidence of accelerated biological aging even in this relatively young cohort. Receiver operating characteristic analysis demonstrated modest discriminatory performance area under the curve = 0.698 (95% CI: 0.60-0.79). Notably, across all inheritance models, TERF1 and TERF2 polymorphisms exhibited no significant association with LTL. Furthermore, subgroup analyses revealed that LTL attrition was independent of chronological age, sex, smoking status, or disease duration, indicating that telomere erosion is driven primarily by intrinsic disease-related systemic stress rather than host shelterin genetic predisposition.
CONCLUSIONS: Our findings demonstrate that leukocyte telomere shortening represents a distinct molecular signature of premature biological aging in young MS patients. By decoupling telomere depletion from primary shelterin genetic variability, this work consistent with disease-driven immunosenescence in MS. In long-standing, heterogeneous disorders like MS, LTL emerges as a promising biomarker for capturing biological decline prior to irreversible neurodegeneration. This study provides a basis for future longitudinal multi-omics investigations exploring telomere dynamics in chronic neuroinflammation.