ArticleJCI insight2016
Activity of Na
Article in JCI insight, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 40 citations in OpenAlex.
- Nonsense-mediated decay influences position-dependent effects of SCN2A premature stop codons on neuronal excitability and behavior.Molecular psychiatry · 2026Article
- Altered oligodendroglial cell development and increased myelination in SCN2A gain-of-function-linked epilepsy.Acta neuropathologica communications · 2026Article
- Review
- Transgenic mouse models of sodium and potassium channelopathies in epilepsy: insights into disease mechanisms and therapeutics.Bioscience reports · 2025Review
- SCN2A gene mutations with epilepsy: single center experience.Italian journal of pediatrics · 2025Article
- 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
- DecipheringArXiv · 2024Article
- Aberrant hippocampal CaeLife · 2024Article
- The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024Review
- Aberrant hippocampal CabioRxiv : the preprint server for biology · 2024Article
- Dependence of cortical neuronal strength-duration properties on TMS pulse shape.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2023Article
- Blockers of Skeletal Muscle NaInternational journal of molecular sciences · 2023Review
- Cellular and behavioral effects of altered NaV1.2 sodium channel ion permeability in Scn2aK1422E mice.Human molecular genetics · 2022Article
- Neuronal Adenosine AFrontiers in cellular neuroscience · 2022Article
- Antisense oligonucleotide therapy reduces seizures and extends life span in an SCN2A gain-of-function epilepsy model.The Journal of clinical investigation · 2021Article
- Sodium channelopathies of skeletal muscle and brain.Physiological reviews · 2021Review
- Ion Channels as New Attractive Targets to Improve Re-Myelination Processes in the Brain.International journal of molecular sciences · 2021Review
- Sodium channelopathies in neurodevelopmental disorders.Nature reviews. Neuroscience · 2021Review
- Theoretical and Therapeutic Implications of the Spasticity-Plus Syndrome Model in Multiple Sclerosis.Frontiers in neurology · 2021Article
- Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?Frontiers in cellular neuroscience · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Counteracting the progressive neurological disability caused by neuronal and axonal loss is the major unmet clinical need in multiple sclerosis therapy. However, the mechanisms underlying irreversible neuroaxonal degeneration in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) are not well understood. A long-standing hypothesis holds that the distribution of voltage-gated sodium channels along demyelinated axons contributes to neurodegeneration by increasing neuroaxonal sodium influx and energy demand during CNS inflammation. Here, we tested this hypothesis in vivo by inserting a human gain-of-function mutation in the mouse Na
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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.