TRE may be particularly well-suited for use in the HD population because of its ability to induce autophagy and clear mHTT, upregulate Sirtuin 1 (SIRT1) and stimulate brain-derived neurotrophic factor (BDNF) production, improve mitochondrial bioenergetics and prevent oxidative stress via mediation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and regulate circadian function. This evidence concerns the gene PPARGC1A and Huntington disease.