c‑Jun N‑terminal kinase 3 signalling serves a potential role as a biomarker for determining the pathogenesis of Parkinson's disease.

Parkinson's disease (PD) is a movement-associated disorder that specifically affects dopamine-producing neurons. The disease causes demyelation that adversely impacts upon the motor activity of the brain. Currently there are no promising biomarkers for PD; improved understanding of the molecular mechanisms underlying the different pathological stages of PD are required to enable identification of a novel biomarker. The present study successfully established a PD mouse model via nasal injection of 1‑methyl-4‑phenyl-1,2,3,6-tetrahydropyridine. The expression of c‑Jun N‑termal kinase 3 (JNK3) and caspase‑3 in two different pathological stages of PD were analysed using immunohistochemistry and western blot analysis. The results inidcated that the initial PD pathogenesis recovers on response to rasagiline. Immunohistochemistry and western blot analysis revealed that treatment with rasagiline positively regulated early‑stage PD pathogenesis by downregulating the expression of JNK3 and upregulating caspase‑3; however, there was no positive effect on the advanced stages of PD. Overall, these results concluded that rasagiline has the ability to inhibit the expression of JNK3 and upregulate caspase‑3 in early stages of PD; however, rasagline appears to have no impact on JNK3 and caspase‑3 levels in the advanced stages of PD.