ReviewBrain pathology (Zurich, Switzerland)2007
Sodium channels and multiple sclerosis: roles in symptom production, damage and therapy.
Review in Brain pathology (Zurich, Switzerland), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 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
46 citing papers in PubMed, 116 citations in OpenAlex.
- Ectopic sodium channel expression decreases excitability of Drosophila Kenyon cells.The Journal of physiology · 2025Article
- Review
- A metformin add-on clinical study in multiple sclerosis to evaluate brain remyelination and neurodegeneration (MACSiMiSE-BRAIN): study protocol for a multi-center randomized placebo controlled clinical trial.Frontiers in immunology · 2024Article
- Optic nerve diseases and regeneration: How far are we from the promised land?Clinical & experimental ophthalmology · 2023Review
- Compromised Myelin and Axonal Molecular Organization Following Adult-Onset Sulfatide Depletion.Biomedicines · 2023Article
- Neuron-oligodendrocyte potassium shuttling at nodes of Ranvier protects against inflammatory demyelination.The Journal of clinical investigation · 2023Article
- Optic Neuritis in Multiple Sclerosis-A Review of Molecular Mechanisms Involved in the Degenerative Process.Current issues in molecular biology · 2022Review
- Thermal dysregulation in patients with multiple sclerosis during SARS-CoV-2 infection. The potential therapeutic role of exercise.Multiple sclerosis and related disorders · 2022Review
- The Cuprizone Model: Dos and Do Nots.Cells · 2020Review
- Article
- Impaired Thermoregulatory Function during Dynamic Exercise in Multiple Sclerosis.Medicine and science in sports and exercise · 2019Article
- An Overview of the Intrinsic Role of Citrullination in Autoimmune Disorders.Journal of immunology research · 2019Review
- Potential of Sodium MRI as a Biomarker for Neurodegeneration and Neuroinflammation in Multiple Sclerosis.Frontiers in neurology · 2019Review
- Using the Anterior Visual System to Assess Neuroprotection and Remyelination in Multiple Sclerosis Trials.Current neurology and neuroscience reports · 2018Review
- Impaired sweating responses to a passive whole body heat stress in individuals with multiple sclerosis.Journal of neurophysiology · 2017Article
- Elevated intracellular NaJournal of neurochemistry · 2017Article
- The Segregated Expression of Voltage-Gated Potassium and Sodium Channels in Neuronal Membranes: Functional Implications and Regulatory Mechanisms.Frontiers in cellular neuroscience · 2017Article
- Sodium MRI in Multiple Sclerosis is Compatible with Intracellular Sodium Accumulation and Inflammation-Induced Hyper-Cellularity of Acute Brain Lesions.Scientific reports · 2016Article
- Thalamocortical-auditory network alterations following cuprizone-induced demyelination.Journal of neuroinflammation · 2016Article
- Sodium MRI of multiple sclerosis.NMR in biomedicine · 2016Review
Corrections and comments
- Erratum issued
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Our understanding of the potential role of sodium channels in multiple sclerosis (MS) has grown substantially in recent years. The channels have long had a recognized role in the symptomatology of the disease, but now also have suspected roles in causing permanent axonal destruction, and a potential role in modulating the intensity of immune activity. Sodium channels might also provide an avenue to achieve axonal and neuronal protection in MS, thereby impeding the otherwise relentless advance of permanent neurological deficit. The symptoms of MS are largely determined by the conduction properties of axons and these, in turn, are largely determined by sodium channels. The number, subtype and distribution of the sodium channels are all important, together with the way that channel function is modified by local factors, such as those resulting from inflammation (eg, nitric oxide). Suspicion is growing that sodium channels may also contribute to the axonal degeneration primarily responsible for permanent neurological deficits. The proposed mechanism involves intra-axonal sodium accumulation which promotes reverse action of the sodium/calcium exchanger and thereby a lethal rise in intra-axonal calcium. Partial blockade of sodium channels protects axons from degeneration in experimental models of MS, and therapy based on this approach is currently under investigation in clinical trials. Some recent findings suggest that such systemic inhibition of sodium channels may also promote axonal protection by suppressing inflammation within the brain.
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.