ArticlePLoS biology2020
Neuroinflammation in the normal-appearing white matter (NAWM) of the multiple sclerosis brain causes abnormalities at the nodes of Ranvier.
Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- MRI-Based Quantitative Assessment of Normal-Appearing White and Gray Matter Demyelination in Multiple Sclerosis, Parkinson's Disease, Long COVID, and Normal Aging.Biomedicines · 2026Article
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- Label-free tracking of subcortical white matter degradationBiomedical optics express · 2026Article
- Mapping the secondary response to traumatic brain injury using spatial transcriptomics shows acute 4-aminopyridine treatment mitigates axonal and molecular pathology.Acta neuropathologica communications · 2026Article
- Sterol imbalances and cholesterol-24-hydroxylase dysregulation is linked to the underlying progression of multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2025Article
- A focus on the normal-appearing white and gray matter within the multiple sclerosis brain: a link to smoldering progression.Acta neuropathologica · 2025Review
- Multiple sclerosis: what have we learned and can we still learn from electron microscopy.Cellular and molecular life sciences : CMLS · 2025Review
- A Window into New Insights on Progression Independent of Relapse Activity in Multiple Sclerosis: Role of Therapies and Current Perspective.International journal of molecular sciences · 2025Review
- Microglia-orchestrated neuroinflammation and synaptic remodeling: roles of pro-inflammatory cytokines and receptors in neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Multiple sclerosis: etiology in the context of neurovascular unit and immune system involvement and advancements withFrontiers in immunology · 2025Review
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- Differential Expression of PACAP/VIP Receptors in the Post-Mortem CNS White Matter of Multiple Sclerosis Donors.International journal of molecular sciences · 2024Article
- Physiological aging and inflammation-induced cellular senescence may contribute to oligodendroglial dysfunction in MS.Acta neuropathologica · 2024Article
- Article
- Microglia activation in periplaque white matter in multiple sclerosis depends on age and lesion type, but does not correlate with oligodendroglial loss.Acta neuropathologica · 2023Article
- Spatial transcriptomics and neurofilament light chain reveal changes in lesion patterns in murine autoimmune neuroinflammation.Journal of neuroinflammation · 2023Article
- Node of Ranvier remodeling in chronic psychosocial stress and anxiety.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Adult-onset depletion of sulfatide leads to axonal degeneration with relative myelin sparing.Glia · 2023Article
- Pathological ultrastructural alterations of myelinated axons in normal appearing white matter in progressive multiple sclerosis.Acta neuropathologica communications · 2023Article
- The Node of Ranvier as an Interface for Axo-Glial Interactions: Perturbation of Axo-Glial Interactions in Various Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Changes to the structure of nodes of Ranvier in the normal-appearing white matter (NAWM) of multiple sclerosis (MS) brains are associated with chronic inflammation. We show that the paranodal domains in MS NAWM are longer on average than control, with Kv1.2 channels dislocated into the paranode. These pathological features are reproduced in a model of chronic meningeal inflammation generated by the injection of lentiviral vectors for the lymphotoxin-α (LTα) and interferon-γ (IFNγ) genes. We show that tumour necrosis factor (TNF), IFNγ, and glutamate can provoke paranodal elongation in cerebellar slice cultures, which could be reversed by an N-methyl-D-aspartate (NMDA) receptor blocker. When these changes were inserted into a computational model to simulate axonal conduction, a rapid decrease in velocity was observed, reaching conduction failure in small diameter axons. We suggest that glial cells activated by pro-inflammatory cytokines can produce high levels of glutamate, which triggers paranodal pathology, contributing to axonal damage and conduction deficits.
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Registered trials
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