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- W1736017783 startingPage "64" @default.
- W1736017783 abstract "Canine degenerative myelopathy (CDM) represents a unique naturally occurring animal model for human amyotrophic lateral sclerosis (ALS) because of similar clinical signs, neuropathologic findings, and involvement of the superoxide dismutase 1 (SOD1) mutation. A definitive diagnosis can only be made postmortem through microscopic detection of axonal degeneration, demyelination and astroglial proliferation, which is more severe in the dorsal columns of the thoracic spinal cord and in the dorsal portion of the lateral funiculus. Interestingly, the muscle acetylcholine receptor complexes are intact in CDM prior to functional impairment, thus suggesting that muscle atrophy in CDM does not result from physical denervation. Moreover, since sensory involvement seems to play an important role in CDM progression, a more careful investigation of the sensory pathology in ALS is also warranted. The importance of SOD1 expression remains unclear, while oxidative stress and denatured ubiquinated proteins appear to play a crucial role in the pathogenesis of CDM. In this updated narrative review we performed a systematic search of the published studies on CDM that may shed light on the pathophysiological mechanisms of human ALS. A better understanding of the factors that determine the disease progression in CDM may be beneficial for the development of effective treatments for ALS." @default.
- W1736017783 created "2016-06-24" @default.
- W1736017783 creator A5002315707 @default.
- W1736017783 creator A5030489393 @default.
- W1736017783 creator A5057425632 @default.
- W1736017783 creator A5058096682 @default.
- W1736017783 creator A5067787993 @default.
- W1736017783 creator A5076045134 @default.
- W1736017783 creator A5086407082 @default.
- W1736017783 creator A5090034872 @default.
- W1736017783 date "2016-02-01" @default.
- W1736017783 modified "2023-10-16" @default.
- W1736017783 title "Canine degenerative myelopathy: a model of human amyotrophic lateral sclerosis" @default.
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