The proposed research addresses whether aberrant activity of a key information processor in the microglial cells of the brain contributes to the pathogenesis of Alzheimer’s disease. This protein, called Protein Kinase C-eta (PKC-eta), “translates” cues to maintain homeostasis in inflammatory signaling. We will analyze genetic mutations identified in the Genes to Therapies™ program by Rudolph Tanzi, Ph.D., to understand how the mutation alters information processing, with the goal of determining whether PKC-eta is a promising new therapeutic target in Alzheimer’s disease.
