Figure 1.

Model of the pathogenesis of Parkinson’s disease. The central step in Parkinson’s disease pathogenesis is proposed to be the accumulation of alpha-synuclein, while the regular function of alpha-synuclein (SNCA) might involve the formation of vesicles, like GAK. Mitochondrial maintenance and response to oxidative stress are to some extent regulated by DJ1, PINK1, parkin, and HTRA2. Five genes are involved in degradation pathways, either over the lysosome or the ubiquitin-proteasomal complex. If one component in these pathways is disturbed, this might lead to dysfunction of the other components.