From EurekAlert!: "In the vast majority of Parkinson's disease (PD) patients, the disorder arises not because of a genetic defect, but because some external insult triggers the death of dopamine-producing neurons. Now, researchers have reported progress in understanding the mechanism underlying that death ... a cellular switch called Cdk5 [regulates] yet another enzyme called Prx2. This enzyme [acts] to render harmless the chemically active reactive oxygen species that are produced inside mitochondria ... the loss of Prx2 activity also plays a role in human PD. They found reduced Prx2 activity in brain tissue from PD patients. ... our findings suggest that strategies to modulate Prx2 activity serve as beneficial targets for treatment of PD. This is of particular importance since Cdk5 is thought to have normal beneficial roles in neurons and modulating a relevant downstream target rather than Cdk5 directly may be a better therapeutic strategy with regard to this pathway." Interesting - recall that targeting antioxidants to the mitochondria extends life in mice, and recall the important role played by mitochondrial free radicals and reactive oxygen species in aging. More potential here than just a Parkinson's therapy, perhaps.