Neuroprotective mechanism of melatonin on ATP13A2-deficient Parkinson’s disease in vitro model: a proteomics analysis

Parkinson’s disease (PD) is second most common neurodegenerative disorder. Mutations in ATP13A2 gene have been implicated in familial forms of PD but the precise molecular mechanisms associated with the development of disease condition remain unknown. To address this question, ATP13A2-deficient in vitro PD model was developed to identify the dysregulated proteins that impaired autophagy and stress response pathways, which resulted in the imbalance of cellular redox and protein homeostasis. This study further explores the use of melatonin to rescue these changes in ATP13A2-deficient PD model. Indeed, melatonin was able to exert neuroprotective roles by regulating the pathogenic signalling pathways.