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Despite advances in understanding the pathogenesis of Huntington’s disease (HD), there is no effective treatment. In the HD transgenic mouse, expression of a dominant-negative caspase-1 mutant extended survival and delayed the onset of symptoms, suggesting that caspase-1 is crucial in HD pathogenesis.1 In fact, the caspase inhibitor minocycline delayed disease progression and extended survival by 14% in the HD mouse model.2 Minocycline is a second-generation tetracycline commonly used for a prolonged period to treat acne. Minocycline crosses the blood–brain barrier and inhibits caspase-1 in acute stroke and decreases infarct size in a mouse stroke model.2 Minocycline protects neurons in mixed spinal cord cultures …
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