ReviewCurrent opinion in pharmacology2022
Breaking the barriers to remyelination in multiple sclerosis.
Review in Current opinion in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled 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.
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
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.
- The dual role of mTOR in multiple sclerosis pathophysiology: a systematic review.Journal of neurology · 2026Pooled it
- Genome-wide association study provides insights into the genetic basis of Lewy body dementia.Molecular psychiatry · 2025Pooled it
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Deletion ofBiology · 2026Article
- Review
- The hypoxia-inflammation cycle as a key mechanism of smoldering inflammation and progression in multiple sclerosis.Acta neuropathologica · 2026Review
- Adjunctive strategies in multiple sclerosis treatment: non-pharmacological approaches and their potential clinical implications.Journal of translational medicine · 2026Review
- The Cell-Specific Effects of the Human Remyelination-Promoting rHIgM22 on Sphingolipid Metabolism in Cultured Glial Cells.Neurochemical research · 2026Article
- Dual-Targeting miR-219 and miR-146a in Multiple Sclerosis: Bridging Myelin Repair and Neuroinflammation for Novel Therapeutic Insights.Cellular and molecular neurobiology · 2026Review
- Selective GPR17 antagonism enhances structural and functional recovery in animal models of demyelination.PloS one · 2026Article
- Review
- Review
- Review
- The refined Pathways to Cures Research Roadmap for multiple sclerosis cures.Multiple sclerosis (Houndmills, Basingstoke, England) · 2024Article
- Primary Progressive Multiple Sclerosis-A Key to Understanding and Managing Disease Progression.International journal of molecular sciences · 2024Review
- A Phase 1b, Open-Label Study to Evaluate the Safety and Tolerability of the Putative Remyelinating Agent, Liothyronine, in Individuals with MS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- The Effects of NLY01, a Novel Glucagon-Like Peptide-1 Receptor Agonist, on Cuprizone-Induced Demyelination and Remyelination: Challenges and Future Perspectives.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Synthesis and Comprehensive in Vivo Activity Profiling of Olean-12-en-28-ol, 3β-Pentacosanoate in Experimental Autoimmune Encephalomyelitis: A Natural Remyelinating and Anti-Inflammatory Agent.Journal of natural products · 2023Article
- Animal models to investigate the effects of inflammation on remyelination in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Chronically demyelinated axons are rendered susceptible to degeneration through loss of trophic support from oligodendrocytes and myelin, and this process underlies disability progression in multiple sclerosis. Promoting remyelination is a promising neuroprotective therapeutic strategy, but to date, has not been achieved through simply promoting oligodendrocyte precursor cell differentiation, and it is clear that a detailed understanding of the molecular mechanisms underlying failed remyelination is required to guide future therapeutic approaches. In multiple sclerosis, remyelination is impaired by extrinsic inhibitory cues in the lesion microenvironment including secreted effector molecules released from compartmentalized immune cells and reactive glia, as well as by intrinsic defects in oligodendrocyte lineage cells, most notably increased metabolic demands causing oxidative stress and accelerated cellular senescence. Promising advances in our understanding of the cellular and molecular mechanisms underlying these processes offers hope for strategically designed interventions to facilitate remyelination thereby resulting in robust clinical benefits.
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.