However, it has been shown that COX-2 is up-regulated in brain dopaminergic neurons of both PD postmortem specimens and 1-methyl-4-phenyl-1,2,3,6-tertrahydropyridine (MPTP) mouse model of PD, and COX-2 inhibition prevents the formation of the oxidant species dopamine-quinone involved in the pathogenesis of PD, suggesting that the inhibition of COX-2 may be a valuable target for the development of new therapies for PD aimed at slowing the progression of the neurodegenerative process (61). This evidence concerns the gene PTGS2 and Parkinson disease.