Objective/Rationale:
Tobacco and coffee users develop Parkinson’s disease at a significantly lower frequency than the general public. While there are several possible interpretations of these findings, we hypothesize that tobacco and coffee contain chemicals that confer protection from developing PD.
Project Description:
We will test the hypothesis that tobacco and coffee contain chemicals that confer protection from developing PD by using fruit fly models of PD. Our fly models of PD were developed by creating genetic defects in flies that are analogous to some of the genetic defects that cause PD in humans. We will use our PD models to test the ability of tobacco and coffee extracts to prevent nerve cell death, and we will compare the protective effects of tobacco and coffee to nicotine and caffeine, the suspected protective agents of tobacco and coffee, respectively. Fruit flies are ideal for these studies because the very short generation time of flies will allow us to quickly address the neuroprotective potential of tobacco and coffee.
Relevance to Diagnosis/Treatment of Parkinson’s Disease:
Our studies will reveal whether tobacco and coffee contain neuroprotective agents that prevent or delay the onset of PD. If so, we can then proceed to identify the specific chemical agents responsible for these neuroprotective effects. The neuroprotective agents identified from our studies could then be used as treatments to prevent, or delay the progression of PD.
Anticipated Outcome:
The finding that tobacco and coffee users develop PD at a significantly lower frequency than the general public may indicate a preexisting difference in the brains of coffee and tobacco users, or alternatively that coffee and tobacco contain neuroprotective agents that prevent PD. Our studies will help to distinguish between these two models and will also begin to define the chemical agents in tobacco and coffee that are potentially responsible for neuroprotection.
Final Outcome
Dr. Pallanck found that extracts from coffee and tobacco are protective in drosophila alpha-synuclein and parkin models and these effects may be mediated by factors other than caffeine or nicotine. Funding from MJFF facilitated Dr. Pallanck receiving follow-on funding from NIH to continue his work on coffee and tobacco in the form of an R21 award to identify the neuroprotective components of coffee and tobacco and to explore their mechanism of action. Next steps include validating these findings in more sophisticated pre-clinical models of PD.
Publication Based on MJFF Funding:
Trinh, et al. 2010. Decaffeinated Coffee and Nicotine-Free Tobacco Provide Neuroprotection in Drosophila Models of Parkinson’s Disease through an NRF2-Dependent Mechanism. J Neurosci. 2010 Apr 21;30(16):5525-32.
Researchers
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Leo J. Pallanck, PhD