Today, I read an interview with Ted Dawson -- Professor of neurodegenerative diseases and Director of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine -- in which he essentially said the same thing about his recent Parkinson’s disease (PD) research: “…for disease modifying therapy, we are treating patients too late. We really need to treat patients earlier.”
Since AD and PD are both neurodegenerative conditions, it’s not surprising that researchers occasionally travel along the same track… in this case trying to identify likely sufferers sooner in order to begin therapy – hopefully PREVENTIVE therapy – earlier. Once either disease appears, the most we can do – at this time, anyway – is treat the symptoms. Still, I am lucky we’ve come that far.
Of course, different challenges confront scientists working on the two diseases. So far, researchers seem to have a better chance of identifying healthy, but disease-prone candidates for Alzheimer’s studies -- at least in the condition’s early-onset variety -- than for PD. Those afflicted Colombian family members all carry the presenil 1 mutation, which researchers can identify in advance. If there’s a similar, scientific way to tag PD candidates long before symptoms appear, I’m not aware of it. Writes Dawson, “Despite genetic advances in our understanding of PD, it is primarily considered a sporadic disorder with no known cause. “
There’s another difference between the Colombian AD study and Dawson’s recent PD work. In that first case, study participants will receive the drug crenezumab, which researchers hope will prevent the accumulation of amyloid plaques. Dawson’s work involves drug therapy, but also includes induced pluripotent stem (IPS) cells, “teased” from skin cells. I’ve written about that particular technology before.
The brief interview with Dawson about his work with Parkinson’s is very interesting.