ReviewMultiple sclerosis (Houndmills, Basingstoke, England)2019
Remyelination and ageing: Reversing the ravages of time.
Review in Multiple sclerosis (Houndmills, Basingstoke, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 112 citations in OpenAlex.
- Rethinking the Oligodendrocyte Progenitor Cell: One Cell, Many Functions.The European journal of neuroscience · 2026Review
- GPCR-Driven Muscarinic M1 and Histamine H1 Receptor Signaling Converging on the PI3K/Akt/mTOR Pathway: Functional Integration in Neuroinflammation and Myelin Repair in Multiple Sclerosis.Molecular neurobiology · 2026Review
- Neuregulin-1 facilitates myelin regeneration through microglia-mediated mechanisms in a mouse model of chronic demyelination.Nature communications · 2026Article
- Ageing and remyelination failure in people with multiple sclerosis.Brain : a journal of neurology · 2026Review
- Review
- Review
- NMDA receptor antagonists mitigate COVID-19-induced neuroinflammation and improve survival in a mouse model.Scientific reports · 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
- Monocyte-secreted Wnt reduces the efficiency of central nervous system remyelination.PLoS biology · 2025Article
- Enhancing remyelination in multiple sclerosis via M1 muscarinic acetylcholine receptor.Molecular pharmacology · 2025Review
- Senescent-like microglia limit remyelination through the senescence associated secretory phenotype.Nature communications · 2025Article
- Exploratory analysis of biological age measures in a remyelination clinical trial.Brain communications · 2025Article
- The isoflavone puerarin promotes generation of human iPSC-derived pre-oligodendrocytes and enhances endogenous remyelination in rodent models.Journal of neurochemistry · 2025Article
- BrainAgeNeXt: Advancing brain age modeling for individuals with multiple sclerosis.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Demyelination and Remyelination: General Principles.Advances in neurobiology · 2025Review
- Pharmacogenomic screening identifies and repurposes leucovorin and dyclonine as pro-oligodendrogenic compounds in brain repair.Nature communications · 2024Article
- DOR activation in mature oligodendrocytes regulates α-ketoglutarate metabolism leading to enhanced remyelination in aged mice.Nature neuroscience · 2024Article
- Quantifying Remyelination Using χ-Separation in White Matter and Cortical Multiple Sclerosis Lesions.Neurology · 2024Article
- De-escalation and Discontinuation of Disease-Modifying Therapies in Multiple Sclerosis.Current neurology and neuroscience reports · 2024Review
- Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Remyelination is a neuroprotective regenerative response to demyelination that restores saltatory conduction and decreases the vulnerability of axons to irreversible degeneration. It is a highly efficient process: however, as with all regenerative processes, its efficiency declines with ageing. Here we argue that this age-related decline in remyelination has a major impact on the natural history of multiple sclerosis (MS), a disease often of several decades' duration. We describe recent work on (1) how ageing changes the function of oligodendrocyte progenitor cells (OPCs), the cells primarily responsible for generating new myelin-forming oligodendrocytes in remyelination, (2) how these changes are induced by age-related changes in the OPC niche and (3) how these changes can be reversed, thereby opening up the possibility of therapeutically maintaining remyelination efficiency throughout the disease, preserving axonal health and treating the progressive phase of MS.
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.