Abstract: Different forms of programmed cell death have been described to participate in the degeneration of dopaminergic neurons in Parkinson’s disease (PD). Given the critical role that disturbance of mitochondrial homeostasis plays in the pathogenesis of PD, apoptosis can be reasonably considered as one of the cell death pathways involved in neuronal loss (Schon and Przedborski, 2011). Multiple lines of evidence support that proposal such as the observations in postmortem human brain samples of PD patients including mitochondrial complex I deficiency, reactive oxygen species generation, and oxidative damage to lipids, proteins, and DNA, among others. Active forms of caspase-8, -9 and -3, the ultimate executor apoptotic caspase, have also been detected in nigrostriatal dopaminergic neurons in the brains of PD patients. Therefore, a relevant question in the field is whether the blockage of the apoptotic pathway would be able to prevent cell death and become a therapeutical option for this disease.