HTT and Huntington disease: In parallel to the accumulating evidence suggesting HD is a disease of the body, a broad molecular reach for mutant huntingtin has also emerged: energetic dysfunction is suggested by elevated lactate in human HD cortical and striatal regions, abnormalities in Complex II, III, and IV of striatal mitochondria, and metabolic disturbances in glycolytic pathways, sphingolipids, redox signaling, and the tricarboxylic acid (TCA) cycle8–13.