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Mutations in  leucine-rich repeat kinase 2  ( LRRK2 ) have been identified as a genetic cause of familial Parkinson's disease (PD) and have also been found in the more common sporadic form of PD, thus positioning LRRK2 as important in the pathogenesis of PD. Biochemical studies of the disease-causing mutants of LRRK2 implicates an enhancement of kinase activity as the basis of neuronal toxicity and thus possibly the pathogenesis of PD due to LRRK2 mutations. Previously, a chemical library screen identified inhibitors of LRRK2 kinase activity. Here, two of these inhibitors, GW5074 and sorafenib, are shown to protect against G2019S LRRK2-induced neurodegeneration  in vivo  in  Caenorhabditis elegans  and in  Drosophila . These findings indicate that increased kinase activity of LRRK2 is neurotoxic and that inhibition of LRRK2 activity can have a disease-modifying effect. This suggests that inhibition of LRRK2 holds promise as a treatment for PD.

human molecular genetics

Inhibitors of LRRK2 kinase attenuate neurodegeneration and Parkinson-like phenotypes in  Caenorhabditis elegans  and  Drosophila  Parkinson's disease models