Our lab is interested in identifying and understanding the early causative events that influence ‘normal’ age-related cognitive decline as well as memory decline associated with Alzheimer’s disease (AD). To date, pre-clinical work has failed to translate to successful therapeutics for AD. We hypothesize that one key reason for these pre-clinical failures is due to a lack of genetic diversity in mouse models used for discovery and validation of therapeutic targets. To test this hypothesis, our lab has developed the AD-BXDs, the first genetically diverse model of human familial Alzheimer’s disease (FAD). We have shown this model recapitulates multiple aspects of human AD including variable susceptibility to disease, transcriptional changes reminiscent of those observed in the AD human brain, and sensitivity to known AD genetic risk loci. Using this model, we aim to identify specific pathways and drivers that influence resilience versus susceptibility to cognitive decline in AD. My project specifically focuses on neuroinflammation, and investigating the role of microglia in resilience to cognitive decline in AD. I aim to discover and validate a microglial signature that relates to cognitive decline in AD, and exploit this signature to promote resilience.
BS, Chemistry - Biochemistry Specialization, University of Virginia, Charlottesville, VA