Hyperactivation of microglial cells has been implicated in the progression and neuronal injury sustained as a result of several neurodegenerative and inflammatory diseases, many of which are sexually dimorphic. Microglia, mononuclear phagocytic immune cells residing in the CNS, are among the first cell types to respond to neuronal injury. Upon their activation, they synthesize and secrete inflammatory mediators that can be neurotoxic when produced in excess. Therefore, identification of agents that can reduce or prevent their activation is of great clinical importance. The overall goal of my research program is to investigate the cellular and molecular mechanisms regulating microglial phenotype transition and function in the context of CNS pathology and recovery in chronic neuroinflammatory disorders. We focus in particular on identifying key signal transduction and transcription factor activation pathways responsible for controlling microglial inflammatory and neurotrophic gene expression. We also have projects designed to understand microglial regulatory mechanisms in the developing and aging CNS, and how sex influences these processes. Our recent work is aimed at defining microRNAs and histone modifications that contribute to microglial plasticity.
- Joined ERP Program: 2002
- NIH funded
|Current Trainees||Degree Goal|
|No Current ERP Students|
|Past Trainees||Degree Completed|