Parkinson's disease is characterized by the pathologicalloss of dopaminergic neurons in the substantia nigra. The current therapy for Parkinson's disease is aimed to replace the lost transmitter. But the ultimate objective in the neurodegenerative therapy is the functional restoration and/or cessation of progression of neuronal loss. Given the critical role that the c-Jun N-terminal kinase (JNK) pathway plays in regulating the cellular processes that are involved in Parkinson's disease, the importance of JNK in this disease's pathogenesis is being increasingly recognized. Much evidence suggests that JNK plays an important role in mediating 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)/1-methyl-4-phenylpyridnium ion (MPP+)-induced neurotoxicity. Therefore, direct blockade of JNK may prevent or effectively slow the progression of Parkinson's disease. Studies including our own showed that the inhibition of JNK with SP-600125, a specific inhibitor of JNK, protects dopaminergic neurous both from MPP+-induced neuronal apoptosis in vitroand in MPTP Parkinson's disease model. These results support JNK inhibition as a potential strategy in treating Parkinson's disease.