ArticleNeuron2010
Is amyotrophic lateral sclerosis a mitochondrial channelopathy?
Article in Neuron, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 8 citations in OpenAlex.
- AAV-mediated upregulation of VDAC1 rescues the mitochondrial respiration and sirtuins expression in a SOD1 mouse model of inherited ALS.Cell death discovery · 2024Article
- Small Hexokinase 1 Peptide against Toxic SOD1 G93A Mitochondrial Accumulation in ALS Rescues the ATP-Related Respiration.Biomedicines · 2021Article
- Human Pluripotent Stem-Cell-Derived Models as a Missing Link in Drug Discovery and Development.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Human Motor Neurons With SOD1-G93A Mutation Generated From CRISPR/Cas9 Gene-Edited iPSCs Develop Pathological Features of Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2020Article
- Novel function of ceramide for regulation of mitochondrial ATP release in astrocytes.Journal of lipid research · 2018Article
- Differential effects of phytotherapic preparations in the hSOD1 Drosophila melanogaster model of ALS.Scientific reports · 2017Article
Corrections and comments
- Comment on
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
SOD1 is a cause of the fatal, paralytic disorder ALS. Although mechanisms underlying mutant SOD1 neurotoxicity remain uncertain, this protein associates with mitochondria. In this issue of Neuron, Israelson et al. show that mutant SOD1 binds and inhibits the mitochondrial channel VDAC1. This finding sheds light onto possible molecular links between mutant SOD1, mitochondrial dysfunction, and spinal motor neuron degeneration in inherited ALS.
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.