ReviewFrontiers in cellular neuroscience2020
Aging, Cellular Senescence, and Progressive Multiple Sclerosis.
Review in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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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
43 citing papers in PubMed, 75 citations in OpenAlex.
- Myelin Repair as a Neuroprotective Strategy for Multiple Sclerosis: From Bench to Bedside.Medicina (Kaunas, Lithuania) · 2026Review
- Green chemistry for prostate health: exploring nature's toolbox against cancer, inflammation, and hyperplasia.Molecular diversity · 2026Review
- Review
- Accelerated metabolomic aging and its association with social determinants of health in multiple sclerosis.Multiple sclerosis (Houndmills, Basingstoke, England) · 2026Article
- Cellular Senescence in Neurodegeneration: From Cell Types to Therapeutic Opportunities.Biomedicines · 2026Review
- Article
- Article
- Microglia in Brain Aging and Age-Related Diseases: Friends or Foes?International journal of molecular sciences · 2025Review
- Specific GPCRs Elicit Unique Extracellular Vesicle MiRNA Array Signatures: An Exploratory Study.bioRxiv : the preprint server for biology · 2025Article
- The Relevance of Chronological and Biological Aging in the Progression of Multiple Sclerosis.Healthcare (Basel, Switzerland) · 2025Review
- Reversing coma by senolytics and stem cells: the future is now.Journal of translational medicine · 2025Review
- Accelerated Cellular Senescence in Progressive Multiple Sclerosis: A Histopathological Study.Annals of neurology · 2025Article
- Experimental autoimmune encephalomyelitis pathogenesis alters along animal age: impact of S100B expression.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Senescent cell reduction does not improve recovery in mice under experimental autoimmune encephalomyelitis (EAE) induced demyelination.Journal of neuroinflammation · 2025Article
- D-galactose Induces Senescence in Adult Mouse Neural Stem Cells by Imbalanced Oxidant and Antioxidant Activity and Differential Expression of Specific Hub Genes.Molecular neurobiology · 2025Article
- Assessment of relationships between epigenetic age acceleration and multiple sclerosis: a bidirectional mendelian randomization study.Epigenetics & chromatin · 2025Article
- Oligodendroglia in Ageing and Age-Dependent Neurodegenerative Diseases.Advances in neurobiology · 2025Review
- Targeting senescent microglia in progressive multiple sclerosis: a geroscience-informed approach.Frontiers in immunology · 2025Article
- Cellular Senescence in Glial Cells: Implications for Multiple Sclerosis.Journal of neurochemistry · 2025Review
- System-level hypothesis of dopamine imbalance in early multiple sclerosis.Frontiers in neurology · 2025Article
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is one of the most important risk factors for the development of several neurodegenerative diseases including progressive multiple sclerosis (MS). Cellular senescence (CS) is a key biological process underlying aging. Several stressors associated with aging and MS pathology, such as oxidative stress, mitochondrial dysfunction, cytokines and replicative exhaustion are known triggers of cellular senescence. Senescent cells exhibit stereotypical metabolic and functional changes, which include cell-cycle arrest and acquiring a pro-inflammatory phenotype secreting cytokines, growth factors, metalloproteinases and reactive oxygen species. They accumulate with aging and can convert neighboring cells to senescence in a paracrine manner. In MS, accelerated cellular senescence may drive disease progression by promoting chronic non-remitting inflammation, loss or altered immune, glial and neuronal function, failure of remyelination, impaired blood-brain barrier integrity and ultimately neurodegeneration. Here we discuss the evidence linking cellular senescence to the pathogenesis of MS and the putative role of senolytic and senomorphic agents as neuroprotective therapies in tackling disease progression.
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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.