This observation suggests that PGC-1α is emerging as a molecular link between mitochondrial dysfunction and transcriptional dysregulation in PD. In vivo studies have shown that PGC-1α knockouts are much more sensitive to the neurodegenerative effects of MPTP, and increased PGC-1α levels protect neurons from oxidative stress in vitro, α-Syn-mediated cell death in vitro, and MPTP-mediated neuronal degeneration in vivo [72, 73]. The gene discussed is PPARGC1A; the disease is Parkinson disease.