Pathogenic mutations in leucine-rich repeat kinase 2 (LRRK2) are the most frequent cause of genetic Parkinsons disease (PD) known to date. Interestingly, the clinical phenotype of LRRK2 PD patients and sporadic PD cases shows a high degree of similarity. Moreover, single nucleotide polymorphisms at the LRRK2 locus are associated with increased risk to develop sporadic PD. The high prevalence of LRRK2 PD patients worldwide, together with a potential role for LRRK2 in sporadic PD cases strongly underlines the importance of studying LRRK2. Indeed, understanding LRRK2 function in physiological as well as pathological conditions will yield clues for the development of new LRRK2-based therapeutic approaches. In this thesis, we will generate a gamut of tools to study LRRK2 function and dysfunction in vitro and in vivo, which will include an extensive investigation of the link between (pathogenic variants of) LRRK2 and cell viability. In addition, we aim to gain insight in the regulation of cellular LRRK2 phosphorylation by identification of a physiological phosphatase of LRRK2.