ArticleNeurology research international2012
Administration of Recombinant Heat Shock Protein 70 Delays Peripheral Muscle Denervation in the SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis.
Article in Neurology research international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Behavioural effects of oral cannabidiol (CBD) treatment in the superoxide dismutase 1 G93 A (SOD1Psychopharmacology · 2025Article
- Enhanced Interleukin 6 Trans-Signaling Modulates Disease Process in Amyotrophic Lateral Sclerosis Mouse Models.Brain sciences · 2025Article
- Downregulation ofBrain communications · 2025Article
- Extracellular HSPs: The Potential Target for Human Disease Therapy.Molecules (Basel, Switzerland) · 2022Review
- IL6 receptorNeurology(R) neuroimmunology & neuroinflammation · 2019Article
- HSP90 Inhibitor, NVP-AUY922, Improves Myelination in Vitro and Supports the Maintenance of Myelinated Axons in Neuropathic Mice.ACS chemical neuroscience · 2019Article
- Protein-Remodeling Factors As Potential Therapeutics for Neurodegenerative Disease.Frontiers in neuroscience · 2017Review
- Engineering therapeutic protein disaggregases.Molecular biology of the cell · 2016Review
- Type I Vs. Type II Cytokine Levels as a Function of SOD1 G93A Mouse Amyotrophic Lateral Sclerosis Disease Progression.Frontiers in cellular neuroscience · 2015Article
- Barcoding heat shock proteins to human diseases: looking beyond the heat shock response.Disease models & mechanisms · 2014Review
- Characterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part II, results and discussion.Brain and behavior · 2013Article
- Early gene expression changes in spinal cord from SOD1(G93A) Amyotrophic Lateral Sclerosis animal model.Frontiers in cellular neuroscience · 2013Article
- Inducible HSP70 is critical in preventing the aggregation and enhancing the processing of PMP22.ASN neuroArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
A prominent clinical feature of ALS is muscle weakness due to dysfunction, denervation and degeneration of motoneurons (MNs). While MN degeneration is a late stage event in the ALS mouse model, muscle denervation occurs significantly earlier in the disease. Strategies to prevent this early denervation may improve quality of life by maintaining muscle control and slowing disease progression. The precise cause of MN dysfunction and denervation is not known, but several mechanisms have been proposed that involve potentially toxic intra- and extracellular changes. Many cells confront these changes by mounting a stress response that includes increased expression of heat shock protein 70 (Hsp70). MNs do not upregulate Hsp70, and this may result in a potentially increased vulnerability. We previously reported that recombinant human hsp70 (rhHsp70) injections delayed symptom onset and increased lifespan in SOD1(G93A) mice. The exogenous rhHsp70 was localized to the muscle and not to spinal cord or brain suggesting it modulates peripheral pathophysiology. In the current study, we focused on earlier administration of Hsp70 and its effect on initial muscle denervation. Injections of the protein appeared to arrest denervation with preserved large myelinated peripheral axons, and reduced glial activation.
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Registered trials
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