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Huntington's Disease: Astrocytes Shift to Fatty Acid Metabolism
1Department of Pharmacology and Chemical Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA; UPMC Hillman Cancer Center, University of Pittsburgh, PA 15213, USA.
Trends in Endocrinology and Metabolism: TEM
|August 11, 2019
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.