Pyruvate slows disease progression in a G93A SOD1 mutant transgenic mouse model.
Neurosci Lett
; 413(3): 265-9, 2007 Feb 21.
Article
em En
| MEDLINE
| ID: mdl-17174029
ABSTRACT
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.
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Base de dados:
MEDLINE
Assunto principal:
Superóxido Dismutase
/
Ácido Pirúvico
/
Esclerose Lateral Amiotrófica
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article