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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

11.6K

What telomeres teach us about MS

Annalise E Miner1, Jennifer S Graves1

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

Multiple Sclerosis and Related Disorders
|August 9, 2021
PubMed

Insights

Biological age, measured by telomere length (TL), offers insight into multiple sclerosis (MS) progression. Leukocyte telomere length (LTL) correlates with disability and may help target aging pathways to slow MS advancement.

Area of Science:

  • Neuroimmunology
  • Aging Research
  • Multiple Sclerosis Pathophysiology

Background:

  • Patient age significantly influences multiple sclerosis (MS) disease phenotype, with younger patients experiencing relapses and older patients facing progressive disability.
  • Chronological age is a limited predictor of MS progression; biological age may offer greater precision.
  • Telomere length (TL), particularly leukocyte telomere length (LTL), is a recognized biomarker for biological aging and has been linked to aging-related diseases.

Purpose of the Study:

  • To explore the role of biological aging, specifically telomere length, in the progression of multiple sclerosis (MS).
  • To investigate whether leukocyte telomere length (LTL) can serve as a biomarker for MS disability and brain atrophy.
  • To consider reproductive aging factors in conjunction with somatic aging for a comprehensive understanding of MS progression.

Main Methods:

  • Review of existing literature on telomere length (TL) and its correlation with aging processes and diseases.
  • Analysis of studies linking leukocyte telomere length (LTL) to disability levels and brain atrophy in individuals with MS.
  • Consideration of the relationship between reproductive aging markers (e.g., ovarian aging) and somatic aging biomarkers (LTL).

Main Results:

  • Leukocyte telomere length (LTL) is associated with increased disability and brain atrophy in people with MS.
  • LTL accounts for 15% of the association between chronological age and MS disability.
  • Telomere attrition can trigger DNA damage responses and senescence pathways, potentially relevant to chronic autoimmune diseases like MS.

Conclusions:

  • Biological age, assessed via telomere length, provides a more nuanced understanding of MS progression than chronological age alone.
  • Targeting pathways related to biological aging may be crucial for halting non-relapse-related progression in MS.
  • Integrating reproductive aging factors with somatic aging markers may enhance the understanding of MS pathophysiology.

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