S-Space College of Medicine/School of Medicine (의과대학/대학원) Neuroscience (뇌신경과학전공) Journal Papers (저널논문_뇌신경과학전공)
Pyruvate slows disease progression in a G93A SOD1 mutant transgenic mouse model
- Park, J. H.; Hong, Y. H.; Kim, H. J.; Kim, S. M.; Kim, M. J.; Park, K. S.; Sung, J. J.; Lee, K. W.
- Issue Date
- Neurosci Lett. 2007 Feb 21;413(3):265-9. Epub 2006 Dec 13.
- Amyotrophic Lateral Sclerosis/complications/*drug; therapy/mortality/pathology; Analysis of Variance; Animals; Disease Models, Animal; Disease Progression; Gliosis/drug therapy/etiology; Mice; Mice, Transgenic; Psychomotor Performance/drug effects; Pyruvic Acid/*therapeutic use; Spinal Cord/drug effects/metabolism; Superoxide Dismutase/*genetics; Survival Analysis; Tyrosine/analogs & derivatives/metabolism
- Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease caused by selective motor neuron death, and currently no effective treatment is available for ALS. In this study, we investigated the neuroprotective effects of pyruvate, which acts as an anti-oxidant and as an energy source. We treated G93A SOD1 transgenic mice with pyruvate (from 70 days of age, i.p., at 1000 mg/kg/week), and found that it prolonged average lifespan by 12.3 days (10.5%), slowed disease progression, and improved motor performance, but did not delay disease onset. Pyruvate treatment was also associated with reduced nitrotyrosine immunoreactivity, gliosis, and increased Bcl-2 expression in the spinal cords of G93A SOD1 transgenic mice. These results suggest that pyruvate treatment may be a potential therapeutic strategy in ALS.
- 0304-3940 (Print)
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