Bret Stetka, MD; Caroline M. Tanner, MD, PhD


July 02, 2012

In This Article

And Finally, Treatments

Medscape: What potentially disease-modifying agents are under investigation for PD at the moment? Is the free-radical hypothesis still a focus?

Dr. Tanner: It is, yes.One of the compounds being looked at is an agent that elevates uric acid -- not to the gout range, but to high-normal -- because we found that uric acid is inversely associated with risk for PD and also slows PD progression. There's a similar observation that people taking calcium-channel blockers may have a lower risk for disease, so there's a trial ongoing, with the results coming soon.

Other trials have failed to provide unequivocal evidence of an effect on PD progression. There's the selective irreversible monoamine oxidase B inhibitor selegiline, which blocks MPTP, and rasagiline, which has a similar mechanism of action; rasagiline did not receive an indication from the FDA for neuroprotection. Coenzyme Q10, which directly affects the mitochondria, was also recently found to be ineffective.

There's also an ongoing trial on creatine, which also affects mitochondrial function. Finally, a strong inverse association between smoking and PD has been known for decades, and there's a nicotine study starting this year.

Medscape: So, what's next for you and the Parkinson's Institute?

Dr. Tanner: A lot of people investigate genes because it's sexy; the technology gets better and better, and more genes can be identified more quickly and at lower cost with each technological advance. Environmental influences are not easy to assess, and when lifelong exposure information is needed, our current methods involve taking lifelong histories -- no dazzling technology. But we're trying to come up with an equal-opportunity measurement for environmental influences.

One approach is to look at a biomarker: the adverse effect of environmental exposure. For example, I am working with Tim Greenamyre at the University of Pittsburgh, who's developing a marker for impaired mitochondrial function that can be determined with a blood test. We're going back to several of our exposed populations to see whether we can use this marker to identify those who were exposed, either with PD or possibly at risk. This could be immediately applicable in an industrial or occupational setting.

We also hope to extend our screening to investigate people who may be at risk for PD owing to environmental exposures. Now we want to look at people who were exposed to environmental factors associated with an increased risk for PD but don't have disease, to see whether they're exhibiting any pre-Parkinson symptoms, such as impaired olfaction or autonomic nervous system dysfunction. These people, just like those with genetic risk factors, may benefit from lifestyle changes associated with lower risk for PD or, in the future, treatment with a preventive therapy.

I have a public health background, so the bottom line is, I want to prevent this disease.


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