As such, AG not only mitigates the stress-provoked ATP hyperproduction and the associated excessive generation of ROS by burdened mitochondria in a UCP2-driven manner, but also re-invigorates mitoprotective and mitochondrial biogenesis-inducing AMPK and PGC-1α signaling in AD and PD. This evidence concerns the gene PPARGC1A and Parkinson disease.