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Abstract
Pathogenic mutations in leucine-rich repeat kinase 2 (LRRK2) are common genetic causes of late-onset Parkinson’s disease (PD). Initial studies indicated that the intrinsic kinase activity of LRRK2 is associated with LRRK2-mediated PD pathogenesis. However, LRRK2 kinase activity may be dispensable for neuron survival and may not be required for its protective activity against neurotoxicity. Thus, the intrinsic kinase activity of LRRK2 appears to be a Trojan horse for PD, and inhibition of its kinase activity could potentially be therapeutically beneficial.
