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Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease
Annual rept. 1 Oct 2007-30 Sep 2008
MASSACHUSETTS GENERAL HOSPITAL BOSTON
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Continued progress has been made toward each of the Specific Aims SAs 1 and 2 SA 3 completed of our research 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 several environmental agents pesticides, caffeine and estrogen that are leading candidate modulators of PD risk. In Year 4 we have 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 neuroprotection in chronic pesticide and genetic mouse models of PD. Critical to our ability to successfully pursue the Specific Aims of our research program, we have made technical progress in assessing modification of a key conditional KO methodology developed in this project. We have presented initial data applying this method to the MPTP model of neurodegeneration in PD.
APPROVED FOR PUBLIC RELEASE