Journal
HUMAN MOLECULAR GENETICS
Volume 25, Issue 9, Pages 1792-1802Publisher
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddw051
Keywords
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Funding
- National Institutes of Health [ES020766-01, NS060115, CA092584, SC1NS095380, GM061838]
- University of Puerto Rico Infrastructural [MD007600, AG04337601]
- Portuguese Foundation for Science and Technology [SFRH/BPD/97544/2013]
- Fundação para a Ciência e a Tecnologia [SFRH/BPD/97544/2013] Funding Source: FCT
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Oxidative damage to mitochondria (MT) is a major mechanism for aging and neurodegeneration. We have developed a novel synthetic antioxidant, XJB-5-131, which directly targets MT, the primary site and primary target of oxidative damage. XJB-5-131 prevents the onset of motor decline in an HdhQ(150/150) mouse model for Huntington's disease (HD) if treatment starts early. Here, we report that XJB-5-131 attenuates or reverses disease progression if treatment occurs after disease onset. In animals with well-developed pathology, XJB-5-131 promotes weight gain, prevents neuronal death, reduces oxidative damage in neurons, suppresses the decline of motor performance or improves it, and reduces a graying phenotype in treated HdhQ(150/150) animals relative to matched littermate controls. XJB-5-131 holds promise as a clinical candidate for the treatment of HD.
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