Mitochondrial targeting of XJB-5-131 attenuates or improves pathophysiology in HdhQ150 animals with well-developed disease phenotypes

Aris Polyzos(Lawrence Berkeley National Laboratory), Amy Holt(Lawrence Berkeley National Laboratory), Christopher Brown(University of California, Berkeley), Celica Cosme(University of California, Berkeley), Peter Wipf(University of Pittsburgh), Àlex Gómez-Marín(Consejo Superior de Investigaciones Científicas), María del R. Castro(University of Puerto Rico System), Sylvette Ayala‐Peña(University of Puerto Rico System), Cynthia T. McMurray(Lawrence Berkeley National Laboratory)
Human Molecular Genetics
February 21, 2016
Cited by 59Open Access
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Abstract

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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