Understanding LRRK2 kinase activity could be potentially important for putative treatment options of both LRRK2-PD and sporadic PD cases [4], Given that tetrameric, native α-synuclein is resistant to aggregation [30, 38, 39], our data also suggest that LRRK2 kinase inhibitors could have a therapeutic benefit in halting Parkinson’s disease progression and development of nonmotor symptoms by increasing native, presynaptic α-synuclein at membranes and protecting against pathologic aggregation. Here, LRRK2 is linked to Parkinson disease.