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Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease
Annual rept. 1 Oct 2008-30 Sep 2009
MASSACHUSETTS GENERAL HOSPITAL BOSTON
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During the reporting period continued progress has been made toward our original Specific Aims 1-3 through approved Modified Aims M1 and M2 of our project, Caffeine, adenosine receptors and estrogen in toxin models of Parkinsons disease PD. The overarching hypothesis of the project is that multiple environmental protectants and toxins interact to influence of the health of the dopaminergic neurons lost in PD. To that end we are characterizing the interplay between environmental agents e.g., pesticides, caffeine, estrogen that are leading candidate modulators of PD risk. In Year 5 we obtained and reported evidence that the adenosine receptor blocker caffeine as well as specific genetic depletion of the A2A subtype of adenosine receptor are capable of conferring protection against neuron degeneration in chronic pesticide and genetic mouse models of PD. Moreover, we have demonstrated and published that adenosine A2A receptors expressed in forebrain neuron are critical for neuron degeneration in toxin model of PD. We also identified CSF levels of urate an environmentally and genetically determined antioxidant is a predictor of progression of PD.
APPROVED FOR PUBLIC RELEASE