Since impaired mitochondrial function is at the basis of the pathogenesis of almost all NDD, and given the strong evidence for the involvement of PGC-1α in major NDD including AD, PD, HD, and ALS [197], PGC-1α can be considered as a pharmacotherapeutic target in NDD and screening for new anti-neurodegenerative agents [198]. This evidence concerns the gene PPARGC1A and Huntington disease.