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Tracing Parkinson's lethal mechanism

overed evidence that the loss of Prx2 activity also plays a role in human PD. They found reduced Prx2 activity in brain tissue from PD patients.

These findings provide a mechanistic link of how a mitochondrial damaging agent, through calpain-mediated Cdk5 activation and downregulation of an important antioxidant enzyme, can increase oxidative load, leading ultimately to death, concluded the scientists.

Taken together, our findings suggest that strategies to modulate Prx2 activity serve as beneficial targets for treatment of PD, they concluded. 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.


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Contact: Erin Doonan
edoonan@cell.com
617-397-2802
Cell Press
5-Jul-2007


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