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Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis

Telomeres are protective cap structures at the end of chromosomes that are essential for maintaining genomic stability. Accelerated telomere shortening is related to premature cellular senescence. Shortened telomere lengths (TL) have been implicated in the pathogenesis of various chronic immune-medi...

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Autores principales: Bühring, Jan, Hecker, Michael, Fitzner, Brit, Zettl, Uwe Klaus
Formato: Online Artículo Texto
Lenguaje:English
Publicado: JKL International LLC 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8279528/
https://www.ncbi.nlm.nih.gov/pubmed/34341708
http://dx.doi.org/10.14336/AD.2021.0106
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author Bühring, Jan
Hecker, Michael
Fitzner, Brit
Zettl, Uwe Klaus
author_facet Bühring, Jan
Hecker, Michael
Fitzner, Brit
Zettl, Uwe Klaus
author_sort Bühring, Jan
collection PubMed
description Telomeres are protective cap structures at the end of chromosomes that are essential for maintaining genomic stability. Accelerated telomere shortening is related to premature cellular senescence. Shortened telomere lengths (TL) have been implicated in the pathogenesis of various chronic immune-mediated and neurological diseases. We aimed to systematically review the current literature on the association of TL as a measure of biological age and multiple sclerosis (MS). A comprehensive literature search was conducted to identify original studies that presented data on TL in samples from persons with MS. Quantitative and qualitative information was extracted from the articles to summarize and compare the studies. A total of 51 articles were screened, and 7 of them were included in this review. In 6 studies, average TL were analyzed in peripheral blood cells, whereas in one study, bone marrow-derived cells were used. Four of the studies reported significantly shorter leukocyte TL in at least one MS subtype in comparison to healthy controls (p=0.003 in meta-analysis). Shorter telomeres in patients with MS were found to be associated, independently of age, with greater disability, lower brain volume, increased relapse rate and more rapid conversion from relapsing to progressive MS. However, it remains unclear how telomere attrition in MS may be linked to oxidative stress, inflammation and age-related disease processes. Despite few studies in this field, there is substantial evidence on the association of TL and MS. Variability in TL appears to reflect heterogeneity in clinical presentation and course. Further investigations in large and well-characterized cohorts are warranted. More detailed studies on TL of individual chromosomes in specific cell types may help to gain new insights into the pathomechanisms of MS.
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spelling pubmed-82795282021-08-01 Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis Bühring, Jan Hecker, Michael Fitzner, Brit Zettl, Uwe Klaus Aging Dis Review Article Telomeres are protective cap structures at the end of chromosomes that are essential for maintaining genomic stability. Accelerated telomere shortening is related to premature cellular senescence. Shortened telomere lengths (TL) have been implicated in the pathogenesis of various chronic immune-mediated and neurological diseases. We aimed to systematically review the current literature on the association of TL as a measure of biological age and multiple sclerosis (MS). A comprehensive literature search was conducted to identify original studies that presented data on TL in samples from persons with MS. Quantitative and qualitative information was extracted from the articles to summarize and compare the studies. A total of 51 articles were screened, and 7 of them were included in this review. In 6 studies, average TL were analyzed in peripheral blood cells, whereas in one study, bone marrow-derived cells were used. Four of the studies reported significantly shorter leukocyte TL in at least one MS subtype in comparison to healthy controls (p=0.003 in meta-analysis). Shorter telomeres in patients with MS were found to be associated, independently of age, with greater disability, lower brain volume, increased relapse rate and more rapid conversion from relapsing to progressive MS. However, it remains unclear how telomere attrition in MS may be linked to oxidative stress, inflammation and age-related disease processes. Despite few studies in this field, there is substantial evidence on the association of TL and MS. Variability in TL appears to reflect heterogeneity in clinical presentation and course. Further investigations in large and well-characterized cohorts are warranted. More detailed studies on TL of individual chromosomes in specific cell types may help to gain new insights into the pathomechanisms of MS. JKL International LLC 2021-08-01 /pmc/articles/PMC8279528/ /pubmed/34341708 http://dx.doi.org/10.14336/AD.2021.0106 Text en copyright: © 2021 Buhring et al. https://creativecommons.org/licenses/by/2.0/this is an open access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
spellingShingle Review Article
Bühring, Jan
Hecker, Michael
Fitzner, Brit
Zettl, Uwe Klaus
Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis
title Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis
title_full Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis
title_fullStr Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis
title_full_unstemmed Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis
title_short Systematic Review of Studies on Telomere Length in Patients with Multiple Sclerosis
title_sort systematic review of studies on telomere length in patients with multiple sclerosis
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8279528/
https://www.ncbi.nlm.nih.gov/pubmed/34341708
http://dx.doi.org/10.14336/AD.2021.0106
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