ReviewEpilepsia2019
Predicting the impact of sodium channel mutations in human brain disease.
Review in Epilepsia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Voltage-Gated CaFrontiers in synaptic neuroscience · 2021Review
- Channelopathy of Dravet Syndrome and Potential Neuroprotective Effects of Cannabidiol.Journal of central nervous system disease · 2021Review
- MRNA Transcription, Translation, and Defects in Developmental Cognitive and Behavioral Disorders.Frontiers in molecular biosciences · 2020Review
- Review
- Unraveling Dravet Syndrome: Exploring the complex effects of sodium channel mutations on neuronal networks.Science progressArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Genetic alteration of the sodium channel provides a remarkable opportunity to understand how epilepsy and its comorbidities arise from a molecular disease of excitable membranes, and a chance to create a better future for children with epileptic encephalopathy. In a single cell, the channel reliably acts as a voltage-sensitive switch, enabling axon impulse firing, whereas at a network level, it becomes a variable rheostat for regulating dynamic patterns of neuronal oscillations, including those underlying cognitive development, seizures, and even premature lethality. Despite steady progress linking genetic variation of the channels with distinctive clinical syndromes, our understanding of the intervening biologic complexity underlying each of them is only just beginning. More research on the functional contribution of individual channel subunits to specific brain networks and cellular plasticity in the developing brain is needed before we can reliably advance from precision diagnosis to precision treatment of inherited sodium channel disorders.
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.