ArticleJournal of neuroscience research2013
Characterization of intercostal muscle pathology in canine degenerative myelopathy: a disease model for amyotrophic lateral sclerosis.
Article in Journal of neuroscience research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Pathology of general proprioception in a canine disease model of amyotrophic lateral sclerosis.Journal of the neurological sciences · 2026Article
- Tibialis Cranialis Extrafusal and Intrafusal Myofibers and Muscle Spindle Pathology in Canine Degenerative Myelopathy.Animals : an open access journal from MDPI · 2026Article
- Common Neurologic Diseases in Geriatric Dogs.Animals : an open access journal from MDPI · 2024Review
- Exosomal TAR DNA binding protein 43 profile in canine model of amyotrophic lateral sclerosis: a preliminary study in developing blood-based biomarker for neurodegenerative diseases.Annals of medicine · 2023Article
- Characterization of neurological disease progression in a canine model of CLN5 neuronal ceroid lipofuscinosis.Developmental neurobiology · 2022Article
- Electrical Impedance Myography in Dogs With Degenerative Myelopathy.Frontiers in veterinary science · 2022Article
- The Long-Term Clinical Course of Canine Degenerative Myelopathy and Therapeutic Potential of Curcumin.Veterinary sciences · 2021Article
- Neuromuscular Plasticity in a Mouse Neurotoxic Model of Spinal Motoneuronal Loss.International journal of molecular sciences · 2019Article
- Cerebrospinal Fluid Levels of Phosphorylated Neurofilament Heavy as a Diagnostic Marker of Canine Degenerative Myelopathy.Journal of veterinary internal medicine · 2017Article
- Changes in respiratory function in Pembroke Welsh Corgi dogs with degenerative myelopathy.The Journal of veterinary medical science · 2016Article
- From animal models to human disease: a genetic approach for personalized medicine in ALS.Acta neuropathologica communications · 2016Review
- Variants within the SP110 nuclear body protein modify risk of canine degenerative myelopathy.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Intracerebroventricular gene therapy that delays neurological disease progression is associated with selective preservation of retinal ganglion cells in a canine model of CLN2 disease.Experimental eye research · 2016Article
- Characterization of thoracic motor and sensory neurons and spinal nerve roots in canine degenerative myelopathy, a potential disease model of amyotrophic lateral sclerosis.Journal of neuroscience research · 2014Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Dogs homozygous for missense mutations in the SOD1 gene develop a late-onset neuromuscular disorder called degenerative myelopathy (DM) that has many similarities to amyotrophic lateral sclerosis (ALS). Both disorders are characterized by widespread progressive declines in motor functions, accompanied by atrophic changes in the descending spinal cord tracts. Some forms of ALS are also associated with SOD1 mutations. In end-stage ALS, death usually occurs as a result of respiratory failure from severe functional impairment of respiratory muscles. The mechanisms that lead to this loss of function are not known. Dogs with DM are euthanized at all stages of disease progression, providing an opportunity to characterize the onset and progression of any pathological changes in the respiratory muscles that may precede respiratory failure. To characterize such potential disease-related pathology, we evaluated intercostal muscles from Boxer and Pembroke Welsh Corgi dogs that were euthanized at various stages of DM disease progression. DM was found to result in intercostal muscle atrophy, fibrosis, increased variability in muscle fiber size and shape, and alteration in muscle fiber type composition. This pathology was not accompanied by retraction of the motor neuron terminals from the muscle acetylcholine receptor complexes, suggesting that the muscle atrophy did not result from physical denervation. These findings provide a better understanding of the mechanisms that likely lead to respiratory failure in at least some forms of ALS and will be useful in the development and evaluation of potential therapeutic interventions using the DM model.
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