Over the last few years, several genes for monogenic forms of Parkinson's 
disease (PD) have been mapped and/or cloned. Mutations have been identified in 
the gene for alpha-synuclein in rare families with dominant PD, indicating that 
aggregation of this protein in Lewy bodies is probably a crucial step in the 
molecular pathogenesis of the disorder. A much more common cause for dominant 
PD, mutations in the gene for leucine-rich repeat kinase 2 (LRRK2), has recently 
been identified. Mutations in the parkin gene, in DJ-1 and PINK1 all cause 
autosomal recessive parkinsonism of early onset. These genes have been 
implicated in the proteasomal protein degradation pathway, in the oxidative 
stress response and mitochondrial function. Mutations in recessive genes 
probably are pathogenic through loss-of-function mechanisms, suggesting that 
their wildtype 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.