Telomere Length as a biomarker in Multiple Sclerosis
MARIA PIEDRABUENA1, Jorge Correale1, Mauricio Farez1, Marcela Fiol1, Mariano Marrodan1, Celica Ysrraelit1
1FLENI
Objective:
Our purpose is to evaluate two cohorts of patients with MS (PwMS) with different ages but similar disease duration. We measure their LTL and its correlation with clinical and radiological parameters.
Background:
Leukocyte telomere length (LTL) shortens with age as a physiological process and is associated with chronic inflammation and cellular senescence. Therefore, LTL may have an important role in the development and course of multiple sclerosis (MS). We hypothesize that chronologically young MS patients with short telomeres will behave similarly to older MS subjects. 
Design/Methods:
Patients were divided into young (age 18-35 years) and elderly (≥ 50 years). Physical evaluation, 3T brain MRI post-processed with a Deep Learning Software and retinal nerve fiber layer (RNFL) measurement by optical coherence tomography were performed. LTL was measured by quantitative polymerase chain reaction assay.
The Stata program version 15 (Statacorp) was used. Independent t-tests and Pearson’s correlation coefficient were used for continuous variables and chi-squared tests for categorical data.
Results:
105 patients were included (59% females), 56 young and 49 elderly (mean age 28 and 56 years, respectively). Mean disease duration was 5 and 6 years (SD 3.672 and 4.960), respectively. EDSS, T25F, 9HPT, mean RNFL thickness were similar in both groups. As expected, LTL was significantly shorter in older patients [0.60 (0.38-0.89) versus 0.58 (0.47-0.78), p=0.0081]. In elderly patients, LTL correlated with disease duration (p=0.05), EDSS (p=0.006), 9HPT (p=0.0022), brain lesion volume (p=0.0026) and with number of T2 lesions (p=0.01). Interestingly, in young patients, LTL did not correlate with neither clinical nor radiological variables.
Conclusions:
In our study, LTL showed correlation with disability and brain lesion volume only in elderly patients. These findings suggest that different mechanisms of neurodegeneration might be involved in aging PwMS.
10.1212/WNL.0000000000203336