Molecular pathogenesis of Parkinson's disease

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Using transgenic C. elegans that pan-neuronally overexpress human alpha-synuclein in neurons, we searched for genes that modify the neurotoxicity of alpha-synuclein, and identified endocytosis-related genes as modifiers. These results suggest that impairment in endocytotic function is involved in the mechanism of neurodegeneration of PD. We also found that GTP binding is essential to the kinase activity of LRRK2, a responsible gene product of PARK8. We also found that autophosphorylation of Thr1410 and Thr1967 of LRRK2 is important for the regulation of its kinase activity.