Mutations in the LRRK2 gene are the most common genetic cause of Parkinson's disease and lead to increased phosphorylation of RAB proteins by inducing hyperactivity of the LRRK2 enzyme. However, the mechanism by which RAB hyperphosphorylation may contribute to the pathogenesis of Parkinson’s disease is still unclear. In this project, we will investigate in astrocytes and neurons how LRRK2 hyperactivity and increased RAB phosphorylation affect the degradation of damaged mitochondria by autophagy, as disruption of this process has been strongly implicated in the development of Parkinson’s disease. We hope that the results of our work will help to identify new therapeutic targets that can slow down or even halt the progression of Parkinson’s disease.

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