ReviewMolecular neurobiology2016
Antibody-Mediated Oligodendrocyte Remyelination Promotes Axon Health in Progressive Demyelinating Disease.
Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- Current status of neuroprotective and neuroregenerative strategies in multiple sclerosis: A systematic review.Multiple sclerosis (Houndmills, Basingstoke, England) · 2022Pooled it
- The Antibody Dependant Neurite Outgrowth Modulation Response Involvement in Spinal Cord Injury.Frontiers in immunology · 2022Pooled it
- Recognition and management of acute relapse of multiple sclerosis, neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease.Cell death and differentiation · 2026Review
- Targeting Remyelination in Spinal Cord Injury: Insights and Emerging Therapeutic Strategies.CNS neuroscience & therapeutics · 2024Review
- Relapse recovery: The forgotten variable in multiple sclerosis clinical trials.Neurology(R) neuroimmunology & neuroinflammation · 2020Article
- The role of B cells in multiple sclerosis: Current and future therapies.Cellular immunology · 2019Review
- The role of glial-neuronal metabolic cooperation in modulating progression of multiple sclerosis and neuropathic pain.Immunotherapy · 2019Review
- Novel Molecular Leads for the Prevention of Damage and the Promotion of Repair in Neuroimmunological Disease.Frontiers in immunology · 2019Review
- Multiple Sclerosis: Mechanisms of Disease and Strategies for Myelin and Axonal Repair.Neurologic clinics · 2018Review
- Nogo-A Antibodies for Progressive Multiple Sclerosis.CNS drugs · 2017Review
- Recent Advances in Monoclonal Antibody Therapies for Multiple Sclerosis.Expert opinion on biological therapy · 2016Review
- A monoclonal natural human IgM protects axons in the absence of remyelination.Journal of neuroinflammation · 2016Article
- A double-blind, placebo-controlled, single-ascending-dose intravenous infusion study of rHIgM22 in subjects with multiple sclerosis immediately following a relapse.Multiple sclerosis journal - experimental, translational and clinicalArticle
- A double-blind, placebo-controlled, single ascending-dose study of remyelinating antibody rHIgM22 in people with multiple sclerosis.Multiple sclerosis journal - experimental, translational and clinicalArticle
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 1 institution in 1 country.
Funding
Abstract
Demyelination underlies early neurological symptoms in multiple sclerosis (MS); however, axonal damage is considered critical for permanent chronic deficits. The precise mechanisms by which axonal injury occurs in MS are unclear; one hypothesis is the absence or failure of remyelination, suggesting that promoting remyelination may protect axons from death. This report provides direct evidence that promoting oligodendrocyte remyelination protects axons and maintains transport function. Persistent Theiler's virus infection of Swiss Jim Lambert (SJL)/J mice was used as a model of MS to assess the effects of remyelination on axonal injury following demyelination in the spinal cord. Remyelination was induced using an oligodendrocyte/myelin-specific recombinant human monoclonal IgM, rHIgM22. The antibody is endowed with strong anti-apoptotic and pro-proliferative effects on oligodendrocyte progenitor cells. We used (1)H-magnetic resonance spectroscopy (MRS) at the brainstem to measure N-acetyl-aspartate (NAA) as a surrogate of neuronal health and spinal cord integrity. We found increased brainstem NAA concentrations at 5 weeks post-treatment with rHIgM22, which remained stable out to 10 weeks. Detailed spinal cord morphology studies revealed enhanced remyelination in the rHIgM22-treated group but not in the isotype control antibody- or saline-treated groups. Importantly, we found rHIgM22-mediated remyelination protected small- and medium-caliber mid-thoracic spinal cord axons from damage despite similar demyelination and inflammation across all experimental groups. The most direct confirmation of remyelination-mediated protection of descending neurons was an improvement in retrograde transport. Treatment with rHIgM22 significantly increased the number of retrograde-labeled neurons in the brainstem, indicating that preserved axons are functionally competent. This is direct validation that remyelination preserves spinal cord axons and protects functional axon integrity.
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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.