Over the last few years, genetic findings have changed our views on Parkinson's 
disease (PD), as mutations in a growing number of genes are found to cause 
monogenic forms of the disorder. Point mutations in the gene for 
alpha-synuclein, as well as duplications and triplications of the wild-type gene 
cause a dominant form of PD in rare families, pointing towards mishandling of 
this protein as a crucial step in the molecular pathogenesis of the disorder. 
Mutations in the gene for leucine-rich repeat kinase 2 (LRRK2) have recently 
been identified as a much more common cause for dominant PD, while mutations in 
the parkin gene, in DJ-1, PINK1 and ATP13A2 all cause autosomal-recessive 
parkinsonism of early onset. Mutations in recessive genes probably are 
pathogenic through loss-of-function mechanisms, suggesting that their wild-type 
products protect dopaminergic cells against a variety of insults. Evidence is 
emerging that at least some of these genes may play a direct role in the 
etiology of the common sporadic form of PD. Further, it is likely that the 
cellular pathways identified in rare monogenic variants of the disease also shed 
light on the molecular pathogenesis in typical sporadic PD.