ReviewCells2019
The Molecular Basis for Remyelination Failure in Multiple Sclerosis.
Review in Cells, 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, 109 citations in OpenAlex.
- Astrocyte Activation Persists after Recovery of Myelin and Motor Deficits in the Cuprizone Model: a Longitudinal PET and CNS Tissue Analysis Study.Molecular imaging and biology · 2026Article
- Review
- Neurofilaments: A Promising Diagnostic and Prognostic Biomarker in Multiple Sclerosis.Annals of neurosciences · 2026Review
- Article
- Mediterranean Pattern Diet in Multiple Sclerosis: A Review Focusing on Immunometabolites.Current neuropharmacology · 2026Review
- Remyelination therapies are achievable in clinical practice-No.Multiple sclerosis (Houndmills, Basingstoke, England) · 2026Article
- Review
- β-Endorphin Mediates Electroacupuncture-Induced Remyelination via Neural Stem Cell Lineage Modulation in Experimental Autoimmune Encephalomyelitis.CNS neuroscience & therapeutics · 2025Article
- Article
- Oxymatrine possibly inhibits differentiation and maturation of oligodendrocytes in the remyelination of the toxin-induced demyelination animal model.Metabolic brain disease · 2025Article
- From Molecules to Models: miRNAs and Advanced Human Platforms of Neurodegeneration and Repair in Multiple Sclerosis.International journal of molecular sciences · 2025Review
- Apolipoprotein D Expression Dynamics During Cuprizone-Induced Demyelination and Remyelination in a Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2025Article
- Neuroprotective strategies in multiple sclerosis: a status update and emerging paradigms.Expert review of neurotherapeutics · 2025Review
- Exosomes as Biomarkers and Therapeutic Agents in Neurodegenerative Diseases: Current Insights and Future Directions.Molecular neurobiology · 2025Review
- PAK1 regulates oligodendroglial proliferation and repopulation in homeostatic and demyelinating brain.Cellular and molecular life sciences : CMLS · 2025Article
- Deferiprone promoted remyelination and functional recovery through enhancement of oligodendrogenesis in experimental demyelination animal model.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The Dual Role of Microglia in Multiple Sclerosis and its Implications for Diagnostics and Repair.Current neuropharmacology · 2025Review
- The interplay of inflammation and remyelination: rethinking MS treatment with a focus on oligodendrocyte progenitor cells.Molecular neurodegeneration · 2024Review
- Review
- How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024Review
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
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelin sheaths in the central nervous system (CNS) insulate axons and thereby allow saltatory nerve conduction, which is a prerequisite for complex brain function. Multiple sclerosis (MS), the most common inflammatory autoimmune disease of the CNS, leads to the destruction of myelin sheaths and the myelin-producing oligodendrocytes, thus leaving behind demyelinated axons prone to injury and degeneration. Clinically, this process manifests itself in significant neurological symptoms and disability. Resident oligodendroglial precursor cells (OPCs) and neural stem cells (NSCs) are present in the adult brain, and can differentiate into mature oligodendrocytes which then remyelinate the demyelinated axons. However, for multiple reasons, in MS the regenerative capacity of these cell populations diminishes significantly over time, ultimately leading to neurodegeneration, which currently remains untreatable. In addition, microglial cells, the resident innate immune cells of the CNS, can contribute further to inflammatory and degenerative axonal damage. Here, we review the molecular factors contributing to remyelination failure in MS by inhibiting OPC and NSC differentiation or modulating microglial behavior.
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.