My lab investigates the cellular mechanisms underlying functional deficits in dementia and aging. We seek to integrate data from cellular and animal models with data from patients to gain insight into mechanisms of disease and discover new therapeutic targets. We use a variety of approaches, including: rodent behavioral assays, biochemical analysis of genetic mouse models of disease, gene expression with viral vectors, and primary neuronal culture.
Current projects focus on Frontotemporal Dementia (FTD), a devastating neurodegenerative disorder that is a leading cause of dementia before the age of 60. Loss of function mutations in the progranulin gene are one of the most common genetic causes of FTD. We are investigating the cellular function of progranulin, and how progranulin mutations may cause FTD. We are also investigating the role of endolysosomal dysfunction in FTD.
