Author: ["Minghua Chen","Victor O. Ona","Mingwei Li","Robert J. Ferrante","Klaus B. Fink","Shan Zhu","Jie Bian","Lei Guo","Laurie A. Farrell","Steve M. Hersch","Wendy Hobbs","Jean-Paul Vonsattel","Jang-Ho J. Cha","Robert M. Friedlander"]
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Abstract
Huntington disease is an autosomal dominant neurodegenerative disease with no effective treatment. Minocycline is a tetracycline derivative with proven safety. After ischemia, minocycline inhibits caspase-1 and inducible nitric oxide synthetase upregulation, and reduces infarction. As caspase-1 and nitric oxide seem to play a role in Huntington disease, we evaluated the therapeutic efficacy of minocycline in the R6/2 mouse model of Huntington disease. We report that minocycline delays disease progression, inhibits caspase-1 and caspase-3 mRNA upregulation, and decreases inducible nitric oxide synthetase activity. In addition, effective pharmacotherapy in R6/2 mice requires caspase-1 and caspase-3 inhibition. This is the first demonstration of caspase-1 and caspase-3 transcriptional regulation in a Huntington disease model.Cite this article
Chen, M., Ona, V., Li, M. et al. Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease. Nat Med 6, 797–801 (2000). https://doi.org/10.1038/77528 