Question ID: WS-3
Submitted by: Gregory Petsko
January 19, 2011
People afflicted with Alzheimer's, Parkinson's, and Huntington's diseases, as well as Fragile X Syndrome patients, have a significantly lower risk of most cancers (the exception is melanoma, for which there is an increased risk for Parkinson's patients). The converse is also true: cancer survivors are at lower risk for several neurodegenerative diseases. What is the biochemical/cell biology basis for this striking inverse correlation, and can it be exploited for new therapeutic approaches?
| This question has not yet been evaluated by users |
Comments
Submitted By John Baron
Patients with Parkinson's disease tend to be non-smokers; PD is one of the few disorders that smoking protects against. This appears to be a nicotine effect. The expected consequence is a lower risk of many cancers.
Submitted By Felicia Etzkorn
This is really an interesting observation, and deserves further research. At the molecular level, the phosphorylation-dependent cis-trans peptidyl prolyl isomerase, Pin1, is thought to be an anti-cancer drug target, yet there is other evidence that its activity is essential to prevent improper processing of APP to Abeta, which causes Alzheimer's. The second question about exploiting this dichotomy is more difficult. It appears that drug companies exploring Pin1 inhibitors for cancer have abandoned this program; one can speculate on the possibility that anticipated neurological side effects might be the reason. The blood-brain barrier might be one mechanism for exploiting the difference. Felicia Etzkorn
