This work seeks to identify the mechanism underlying prion-induced synaptotoxicity using
genomic, proteomic and pharmacological techniques in mouse and human neurons and in animal models. Specific aims include, defining further the components of prion-induced synaptotoxic pathways in cultured neurons, testing whether reducing p38 MAPK function, either genetically or pharmacologically, ameliorates the symptoms of prion disease in mice, and developing a new model of human prion disease.
