ReviewMultiple sclerosis (Houndmills, Basingstoke, England)2023
Biological aging in multiple sclerosis.
Review in Multiple sclerosis (Houndmills, Basingstoke, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Accelerated Brain Aging Identifies Functional Vulnerability Beyond Chronological Age in Multiple Sclerosis.Sensors (Basel, Switzerland) · 2026Trial
- The role of gut microbiome in aging-associated diseases: where do we stand now and how technology will transform the future.Gut microbes · 2026Review
- Shorter Leukocyte telomere length as a marker of biological aging in relapsing-remitting multiple sclerosis.Acta neurologica Belgica · 2026Article
- Aging with multiple sclerosis and associated prevalence, incidence, comorbidities and healthcare utilization patterns in a population based study.Scientific reports · 2026Article
- From Phenotypes to Spectrum: Rethinking RRMS, SPMS and PPMS in the Era of PIRA-A Framework Integrating PIRA, Smouldering-Associated Worsening, and Neurologic Reserve to Facilitate Earlier Recognition of Progression.Neurology international · 2026Review
- Proteomic Age Acceleration in Multiple Sclerosis Precedes Symptom Onset and Associates with Severity.medRxiv : the preprint server for health sciences · 2026Article
- Telomere length as a marker of biological age in paediatric multiple sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2026Article
- Ageing and remyelination failure in people with multiple sclerosis.Brain : a journal of neurology · 2026Review
- Mediterranean Pattern Diet in Multiple Sclerosis: A Review Focusing on Immunometabolites.Current neuropharmacology · 2026Review
- BAFF is a marker of hypogammaglobulinemia, neuroaxonal damage and inflammation in multiple sclerosis patients on ocrelizumab.Journal of neuroinflammation · 2025Article
- Microglia in Brain Aging and Age-Related Diseases: Friends or Foes?International journal of molecular sciences · 2025Review
- Misalignment of age clocks.GeroScience · 2025Article
- Article
- Inflammation and aging-related disease: A transdisciplinary inflammaging framework.GeroScience · 2025Review
- Review of evidence linking exposure to environmental stressors and associated alterations in the dynamics of immunosenescence (ISC) with the global increase in multiple sclerosis (MS).Immunity & ageing : I & A · 2024Review
- Comparative targeted lipidomics between serum and cerebrospinal fluid of multiple sclerosis patients shows sex and age-specific differences of endocannabinoids and glucocorticoids.Acta neuropathologica communications · 2024Article
- The lung-brain axis in multiple sclerosis: Mechanistic insights and future directions.Brain, behavior, & immunity - health · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is most likely to adopt a progressive clinical course during middle age or beyond, and the number of older adults with MS is steadily increasing. Developing new strategies to manage progressive forms of MS, which do not respond to currently available disease-modifying therapies (DMTs), will require a deeper understanding of the mechanisms by which biological aging interacts with pathogenic pathways to propel disability accumulation. In experimental autoimmune encephalomyelitis (EAE), a widely used preclinical mouse model of MS, middle-aged animals experience a more severe and protracted clinical course than their younger counterparts. This exacerbated disease course is accompanied by persistent neuroinflammation. Clinical studies of age-related biomarkers, such as telomere length, senescence markers, and DNA methylation, suggest that biological aging is accelerated in people with MS compared with age- and sex-matched healthy controls. Furthermore, distinguishing biological age from chronological may afford more precision in determining aging effects in MS. Here we review the current literature on aging biology and its impact on MS pathogenesis. Future research on this topic may lead to the development of novel biomarkers and senotherapy agents that slow neurological decline in people with progressive MS by targeting relevant aging-related pathways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.