ArticleNature neuroscience2025
Mitochondrial respiratory complex IV deficiency recapitulates amyotrophic lateral sclerosis.
Article in Nature neuroscience, 2025. 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 12 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
12 citing papers in PubMed.
- UA-30 ameliorates motor deficits through RalA-mediated mitophagy in ALS mice.The Journal of clinical investigation · 2026Article
- Pml loss worsens NEK1-linked ALS and Pml induction drives NEK1 degradation, precluding disease onset.The FEBS journal · 2026Article
- TDP-43 oxidation and PP1 crosstalk at RNA granule-mitochondria contact sites.Nature communications · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.Nature communications · 2026Article
- Mutant CHCHD10 disrupts cytochrome c oxidation and activates mitochondrial retrograde signaling.EMBO molecular medicine · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.bioRxiv : the preprint server for biology · 2026Article
- Synaptosomes isolated from cryopreserved MND motor cortex reveal altered calcium handling and reduced complex IV-linked respiration.Frontiers in synaptic neuroscience · 2026Article
- Development and efficacy of ex vivo expanded autologous regulatory T cells for the treatment of amyotrophic lateral sclerosis.Frontiers in immunology · 2026Article
- G-Quadruplexes Abet Neuronal Burnout in ALS and FTD.Antioxidants (Basel, Switzerland) · 2025Review
- Cerium-based nanoparticles for neurodegeneration: emerging redox therapeutics beyond pharmaceuticals.RSC advances · 2025Review
- Amyotrophic lateral sclerosis in Mainland China: clinical translational challenges and opportunities.Current opinion in neurology · 2025Review
- A primer on copper biology in the brain.Neurobiology of disease · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
24 authors.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is categorized into ~10% familial and ~90% sporadic cases. While familial ALS is caused by mutations in many genes of diverse functions, the underlying pathogenic mechanisms of ALS, especially in sporadic ALS (sALS), are largely unknown. Notably, about half of the cases with sALS showed defects in mitochondrial respiratory complex IV (CIV). To determine the causal role of this defect in ALS, we used transcription activator-like effector-based mitochondrial genome editing to introduce mutations in CIV subunits in rat neurons. Our results demonstrate that neuronal CIV deficiency is sufficient to cause a number of ALS-like phenotypes, including cytosolic TAR DNA-binding protein 43 redistribution, selective motor neuron loss and paralysis. These results highlight CIV deficiency as a potential cause of sALS and shed light on the specific vulnerability of motor neurons, marking an important advance in understanding and therapeutic development of sALS.
Indexed as
Identifiers
40069360What Socratic 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 Socratic graph.