In rats with PD, CAPE improves scavenging of ROS and metal chelation and inhibits mitochondrial permeability transition (MPT), a mediator of neuronal death that triggers cytochrome c release and caspase-3 activation, but has no effect on brain mitochondrial function, suggesting that CAPE is a potential compound to protect dopaminergic neuronal loss in neurodegenerative diseases [88, 89]. Here, CASP3 is linked to Parkinson disease.