ArticleJournal of neurology2006
Axonal protection achieved in a model of multiple sclerosis using lamotrigine.
Article in Journal of neurology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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.
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Who cites it
40 citing papers in PubMed, 131 citations in OpenAlex.
- Longitudinal changes in magnetisation transfer ratio in secondary progressive multiple sclerosis: data from a randomised placebo controlled trial of lamotrigine.Journal of neurology · 2012Trial
- Hypoxic Neuroinflammation in the Pathogenesis of Multiple Sclerosis.Brain sciences · 2025Review
- Endosomal traffic disorders: a driving force behind neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Tissue Hypoxia and Associated Innate Immune Factors in Experimental Autoimmune Optic Neuritis.International journal of molecular sciences · 2024Article
- Article
- Regulated cell death: discovery, features and implications for neurodegenerative diseases.Cell communication and signaling : CCS · 2021Review
- Neuron-Oligodendrocyte Interactions in the Structure and Integrity of Axons.Frontiers in cell and developmental biology · 2021Review
- The role of glial-neuronal metabolic cooperation in modulating progression of multiple sclerosis and neuropathic pain.Immunotherapy · 2019Review
- Potential of Sodium MRI as a Biomarker for Neurodegeneration and Neuroinflammation in Multiple Sclerosis.Frontiers in neurology · 2019Review
- Clinical applications of ultra-high field magnetic resonance imaging in multiple sclerosis.Expert review of neurotherapeutics · 2018Review
- Regulation and dysregulation of axon infrastructure by myelinating glia.The Journal of cell biology · 2017Review
- Distribution and function of voltage-gated sodium channels in the nervous system.Channels (Austin, Tex.) · 2017Review
- Pharmacological Approaches to the Management of Secondary Progressive Multiple Sclerosis.Drugs · 2017Review
- The influence of sodium on pathophysiology of multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Review
- Experimental autoimmune encephalomyelitis from a tissue energy perspective.F1000Research · 2017Review
- Activity of NaJCI insight · 2016Article
- Sodium channels in astroglia and microglia.Glia · 2016Review
- Sodium MRI of multiple sclerosis.NMR in biomedicine · 2016Review
- Longitudinal Evaluation of Visual Function in Multiple Sclerosis.Optometry and vision science : official publication of the American Academy of Optometry · 2015Article
- Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of multiple sclerosis.Neuroreport · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Axonal degeneration is a major cause of permanent disability in multiple sclerosis (MS). Recent observations from our and other laboratories suggest that sodium accumulation within compromised axons is a key, early step in the degenerative process, and hence that limiting axonal sodium influx may represent a mechanism for axonal protection in MS. Here we assess whether lamotrigine, a sodium channel-blocking agent, is effective in preventing axonal degeneration in an animal model of MS, namely chronic-relapsing experimental autoimmune encephalomyelitis (CR-EAE). When administered from 7 days post-inoculation, lamotrigine provided a small but significant reduction in the neurological deficit present at the termination of the experiments (averaged over three independent experiments; vehicle: 3.5+/-2.7; lamotrigine: 2.6+/-2.0, P<0.05) and preserved more functional axons in the spinal cord (measured as mean compound action potential area; vehicle: 31.7 microV.ms+/-23.0; lamotrigine: 42.9+/-27.4, P<0.05). Histological examination of the thoracic spinal cord (n=71) revealed that lamotrigine treatment also provided significant protection against axonal degeneration (percentage degeneration in dorsal column; vehicle: 33.5 %+/-38.5; lamotrigine: 10.4 %+/-12.5, P<0.01). The findings suggest that lamotrigine may provide a novel avenue for axonal protection in MS.
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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.