Our research focuses on the elucidation of the cellular and molecular events by which mutations in genes linked to Parkinson’s disease (PD) contribute to disease pathology. PD has been classically considered a sporadic disease, however, it is now recognized to have a substantial genetic component. Interestingly, the same genes involved in the autosomal-dominantly inherited forms of PD such as SNCA (a-synuclein), and LRRK2 can act as risk factors in sporadic PD, as well. Given the relevance of LRRK2 and a-synuclein with the sporadic forms of PD, our long-term research goal by interrogating a-synuclein and mainly LRRK2-dependent alterations at the cellular, network and behavioral levels is to understand the pathophysiology of PD. The gained knowledge will provide useful insights towards the development of mechanism-based therapeutic opportunities for a disease that is currently addressed symptomatically.