Abstract Title:

Pyruvate slows disease progression in a G93A SOD1 mutant transgenic mouse model.

Abstract Source:

Neurosci Lett. 2007 Feb 21;413(3):265-9. Epub 2006 Dec 13. PMID: 17174029

Abstract Author(s):

Jong-Ha Park, Yoon-Ho Hong, Hyun-Jung Kim, Sung-Min Kim, Min-Jeong Kim, Kyung-Seok Park, Jung-Joon Sung, Kwang-Woo Lee

Article Affiliation:

Department of Neurology, Seoul National University College of Medicine, Clinical Research Institute of Seoul National University Hospital, 28 Yongon-Dong, Chongno-Gu, Seoul 110-744, South Korea.


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.

Study Type : Transgenic Animal Study

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