ArticleExperimental neurology2012
Absence of SOD1 leads to oxidative stress in peripheral nerve and causes a progressive distal motor axonopathy.
Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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62 citing papers in PubMed, 93 citations in OpenAlex.
- Restoration of circadian rhythm as novel targets against sarcopenia.Chinese medical journal · 2026Review
- Genetic contributions to mitochondrial dysfunction in amyotrophic lateral sclerosis etiology.HGG advances · 2026Article
- Superoxide dismutase impacts extracellular vesicle shedding and uptake.Free radical biology & medicine · 2026Article
- Structural mechanisms and insights on multiple nanobodies binding diverse SOD1 epitopes.Communications biology · 2025Article
- Superoxide dismutase impacts extracellular vesicle biogenesis and uptake.bioRxiv : the preprint server for biology · 2025Article
- RNA-DNA Differences: Mechanisms, Oxidative Stress, Transcriptional Fidelity, and Health Implications.Antioxidants (Basel, Switzerland) · 2025Review
- Skeletal muscle innervation: Reactive oxygen species as regulators of neuromuscular junction dynamics and motor unit remodeling.Free radical biology & medicine · 2025Review
- Rethinking antisense oligonucleotide therapeutics for amyotrophic lateral sclerosis.Annals of clinical and translational neurology · 2024Review
- Review
- Intrathecal administration of a novel siRNA modality extends survival and improves motor function in the SOD1Molecular therapy. Nucleic acids · 2024Article
- Protein aggregation and therapeutic strategies in SOD1- and TDP-43- linked ALS.Frontiers in molecular biosciences · 2024Review
- AAV1.NT-3 gene therapy in the SOD1KO mouse model of accelerated sarcopenia.Journal of cachexia, sarcopenia and muscle · 2023Article
- Pathological insights from amyotrophic lateral sclerosis animal models: comparisons, limitations, and challenges.Translational neurodegeneration · 2023Review
- Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.International journal of molecular sciences · 2023Review
- Dihydromyricetin supplementation during in vitro culture improves porcine oocyte developmental competence by regulating oxidative stress.The Journal of reproduction and development · 2023Article
- The motor system is exceptionally vulnerable to absence of the ubiquitously expressed superoxide dismutase-1.Brain communications · 2023Article
- Sensory Involvement in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2022Review
- Oxidative stress monitoring in iPSC-derived motor neurons using genetically encoded biosensors of HScientific reports · 2022Article
- Characterization of somatosensory neuron involvement in the SOD1Scientific reports · 2022Article
- Heterozygous SOD2 deletion selectively impairs SERCA function in the soleus of female mice.Physiological reports · 2022Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Oxidative stress is commonly implicated in the pathogenesis of motor neuron disease. However, the cause and effect relationship between oxidative stress and motor neuron degeneration is poorly defined. We recently identified denervation at the neuromuscular junction in mice lacking the antioxidant enzyme, Cu,Zn-superoxide dismutase (SOD1) (Fischer et al., 2011). These mice show a phenotype of progressive muscle atrophy and weakness in the setting of chronic oxidative stress. Here, we investigated further the extent of motor neuron pathology in this model, and the relationship between motor pathology and oxidative stress. We report preferential denervation of fast-twitch muscles beginning between 1 and 4 months of age, with relative sparing of slow-twitch muscle. Motor axon terminals in affected muscles show widespread sprouting and formation of large axonal swellings. We confirmed, as was previously reported, that spinal motor neurons and motor and sensory nerve roots in these mice are preserved, even out to 18 months of age. We also found preservation of distal sensory fibers in the epidermis, illustrating the specificity of pathology in this model for distal motor axons. Using HPLC measurement of the glutathione redox potential, we quantified oxidative stress in peripheral nerve and muscle at the onset of denervation. SOD1 knockout tibial nerve, but not gastrocnemius muscle, showed significant oxidation of the glutathione pool, suggesting that axonal degeneration is a consequence of impaired redox homeostasis in peripheral nerve. We conclude that the SOD1 knockout mouse is a model of oxidative stress-mediated motor axonopathy. Pathology in this model primarily affects motor axon terminals at the neuromuscular junction, demonstrating the vulnerability of this synapse to oxidative injury.
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