Mutations in LRRK2 (leucine-rich repeat kinase 2) (also known as PARK8 or 
dardarin) are responsible for the autosomal-dominant form of PD (Parkinson's 
disease). LRRK2 mutations were found in approximately 3-5% of familial and 1-3% 
of sporadic PD cases with the highest prevalence (up to 40%) in North Africans 
and Ashkenazi Jews. To date, mutations in LRRK2 are a major genetic risk factor 
for familial and sporadic PD. Despite the fact that 8 years have passed from the 
establishment of the first link between PD and dardarin in 2004, the 
pathophysiological role of LRRK2 in PD onset and progression is far from clearly 
defined. Also the generation of different LRRK2 transgenic or knockout animals 
has not provided new hints on the function of LRRK2 in the brain. The present 
paper reviews recent evidence regarding a potential role of LRRK2 in the 
regulation of membrane trafficking from vesicle generation to the movement along 
cytoskeleton and finally to vesicle fusion with cell membrane.