Overexpression of PGC‐1α in cerebellar neurons increases mitochondrial density by 30% and protects the neurons against mutant synuclein A53T‐α or mutant Huntingtin gene (Htt)‐induced degeneration.7 The brains of mice lacking PGC‐1α presents microvacuolation and neuronal loss, which highlights the important role of PGC‐1α in the nervous system.8, 9 In fact, the common character of several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, is the impaired function of PGC‐1α. This evidence concerns the gene HTT and juvenile Huntington disease.