Extensive research on these experimental systems together with available PD patients has led to envision a series of molecular mechanisms as accounting for the pathophysiology of PD, including oxidative stress, mitochondrial dysfunction and excitotoxic damage [5,6,11,12], among others including mutations in genes encoding proteins with a neuroprotective role, such as parkin [2,5]. This evidence concerns the gene PRKN and Parkinson disease.