Evidence map›Paper›PMID 41500800›Full record

ArticleJournal of neurology, neurosurgery, and psychiatry2026

Telomere length as a marker of biological age in paediatric multiple sclerosis.

Kayla Jacques, Jonathan Race, Christopher Goyne, Ashley Fair, Allison Schuette, Jennifer H Yang, Stacy Caillier, Gregory Scott Aaen, Aaron Abrams, Leslie Benson and 18 more

Abstract read
In one paragraph

Article in Journal of neurology, neurosurgery, and psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

28 authors.

Kayla JacquesDepartment of Neurosciences, University of California San Diego, La Jolla, California, USA.ORCID http://orcid.org/0009-0006-3841-6142
Jonathan RacePediatrics, The University of Utah, Salt Lake City, Utah, USA.
Christopher GoyneDepartment of Neurosciences, University of California San Diego, La Jolla, California, USA.
Ashley FairDepartment of Neurosciences, University of California San Diego, La Jolla, California, USA.
Allison SchuettePediatrics, The University of Utah, Salt Lake City, Utah, USA.
Jennifer H YangDepartment of Neurosciences, University of California San Diego, La Jolla, California, USA.
Stacy CaillierUniversity of California San Francisco, San Francisco, California, USA.
Gregory Scott AaenLoma Linda University, Loma Linda, California, USA.ORCID http://orcid.org/0000-0002-0408-2053
Aaron AbramsNeurology, Cleveland Clinic, Cleveland, Ohio, USA.ORCID http://orcid.org/0000-0002-4607-5740
Leslie BensonNeurology, Childrens Hospital Boston, Boston, Massachusetts, USA.
T Charles CasperPediatrics, The University of Utah, Salt Lake City, Utah, USA.
Tanuja ChitnisHarvard Medical School, Boston, Massachusetts, USA.
Mark P GormanChildrens Hospital Boston, Boston, Massachusetts, USA.
Tim LotzeBaylor College of Medicine, Houston, Texas, USA.
Lauren KruppPediatric MS Center, NYU Langone Health, New York, New York, USA.ORCID http://orcid.org/0000-0001-7003-807X
Soe MarDepartment of Neurology, Washington University in Saint Louis, St. Louis, Missouri, USA.
Jayne NessUniversity of Alabama at Birmingham, Birmingham, Alabama, USA.
Mary RenselCleveland Clinic, Cleveland, Ohio, USA.
Moses RodriguezNeurology, Mayo Clinic Rochester, Rochester, Minnesota, USA.
John RoseUniversity of Utah Health, Salt Lake City, Utah, USA.
Teri SchreinerDepartment of Neurology, University of Colorado, Aurora, Colorado, USA.
Jan-Mendelt TillemaMayo Clinic, Rochester, Minnesota, USA.
Amy WaldmanThe Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.
Yolanda WheelerDepartment of Nursing, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID http://orcid.org/0000-0003-1391-4496
Jorge OksenbergUniversity of California San Francisco, San Francisco, California, USA.
Jue LinUniversity of California San Francisco, San Francisco, California, USA.
Emmanuelle WaubantUniversity of California San Francisco, San Francisco, California, USA.
Jennifer S GravesDepartment of Neurosciences, University of California San Diego, La Jolla, California, USA jgraves@ucsd.edu.

Funding

Child Neurologist Career Development Program (CNCDP)K12NS098482 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI SCHLAGGAR, BRADLEY L · 2016 to 2025
$26.2M
Environmental and genetic risk factors for pediatric MSR01NS071463 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WAUBANT, EMMANUELLE LAURENCE · 2010 to 2015
$2.8M
NINDS NIH HHS K12 NS098482NINDS NIH HHS R01 NS071463
6 · The paper itself

Abstract

backgroundIncreased chronological age correlates with reduced relapse rates and increased disability in multiple sclerosis (MS). Biological age may better capture ageing's impact on MS and might accelerate due to MS itself. Establishing accelerated biological ageing in adults is complicated by normal ageing and comorbidities. Telomere length, a well-recognised biological ageing marker, is shortened in adults with MS and associated with disability. Demonstrating accelerated biological ageing in paediatric-onset MS (POMS) would strengthen the hypothesis that MS drives premature biological ageing. This study aimed to determine if telomere length differs in POMS compared to age-similar healthy controls.

methodsWe performed a cross-sectional case-control study of whole blood samples and clinical data from The US Network of Pediatric MS Centers. Real-time quantitative PCR measured telomere length, expressed as a telomere to somatic DNA ratio (T/S ratio). T/S ratio was compared between cases and age-similar healthy controls using multivariate regression analysis adjusting for chronological age, sex, race, ethnicity, tobacco exposure, socioeconomic status and body mass index.

resultsWe analysed 300 POMS cases and 200 controls. The unadjusted mean T/S ratios were 1.66 (SD 0.32) for cases and 1.71 (SD 0.29) for controls (mean difference -0.05, 95% CI -0.10 to 0.01, p=0.08). After adjusting for key covariables with face validity, POMS participants had a mean 0.086 shorter T/S ratio than controls (95% CI 0.015 to 0.157, p=0.018).

conclusionsPOMS participants demonstrated shorter telomeres than age-similar controls in a multivariable model adjusting for sociodemographic variables, suggesting that MS may contribute to accelerated biological ageing.

Indexed as

AgingMultiple SclerosisTelomereAdolescentBiomarkersCase-Control StudiesChildCross-Sectional StudiesFemaleHumansMaleBiomarkersGENETICSMULTIPLE SCLEROSISNEUROIMMUNOLOGYPAEDIATRIC NEUROLOGY

Identifiers

PMID41500800
PMCPMC13292612

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.