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In this review, we discuss how familial forms of PD have led us to hypothesize that alterations in endomembrane trafficking play a role in the pathobiology of PD.

We will discuss the major observations that have been made to elucidate the role of LRRK2 in particular, including LRRK2 animal models and high-throughput proteomics approaches.

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These biochemical and structural observations suggest, first, that LRRK2 is a co-ordinated signaling molecule that has linked enzyme activities and potentially multiple protein interaction partners and, second, that mutations associated with PD can modify these activities.

The next important question, is what effects LRRK2 has within cells and, therefore, within the organism.

Taken together, these studies strongly support a role of LRRK2 in vesicular dynamics.

We also propose that targeting these pathways may not only be beneficial for developing therapeutics for LRRK2-driven PD, but also for other familial and sporadic cases.

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