Abstract
A recent study by Polyzos et al. (Cell Metab., 2019) shows that astrocytes in a Huntington disease (HD) mouse model switch from glycolysis to fatty acid oxidation (FAO), causing increased superoxide radical anion production and loss of succinate dehydrogenase (SD) activity. Blocking mitochondria reactive oxygen species (ROS) with an antioxidant compound called XJB-5-151 reversed lipofuscin formation and protected the mice.
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