This proposal addresses whether a key protein that is turned off in cancer, a disease characterized by uncontrolled cellular growth and survival, is excessively active in Alzheimer’s disease, a degenerative disease. This protein, called protein kinase C, is an information processor, or “signal transducer,” that regulates cellular activities. Its activity needs to be precisely balanced to maintain normal cellular function. Reduced function promotes cell survival, a hallmark of cancer. Analysis of genetic mutations identified in the Genes to Therapies™ program by Rudy Tanzi reveals that mutations found in some patients with Alzheimer’s disease enhance the function of protein kinase C. This project examines whether enhanced signaling by protein kinase C generally is associated with the pathology of Alzheimer’s disease, identifying protein kinase C as a promising therapeutic target.
Alzheimer Disease-Associated Mutations in Protein Kinase C
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