I study the role of microglia in amyloid pathology and neuroinflammation in Alzheimer’s disease. My work has shown that the G-protein–coupled receptor GPR3 modulates soluble Aβ levels and influences plaque compaction and burden in a preclinical model of Alzheimer’s disease. These findings suggest that microglial signaling through GPR3 contributes to limiting plaque formation and disease progression. Current efforts are focused on elucidating the molecular mechanisms by which GPR3 regulates microglial responses to amyloid pathology.

I investigated mechanisms underlying microglial activation and metabolic reprogramming during neural injury. My work revealed a link between inhibition of the Hv1 proton channel and alterations in microglial energy metabolism, which in turn promoted neuroprotection under conditions of excitotoxic stress. Using the experimental tools developed in this model, I further examined how aberrant microglial activation influences tissue repair. I found that pro-inflammatory microglial phenotypes impair glial scar formation, highlighting a mechanism by which dysregulated immune responses interfere with CNS recovery.

In collaborative work, I investigated mechanisms linking oxidative stress to neuronal injury in a model of glucose deprivation and calpain activation. My findings demonstrated that NOX-derived reactive oxygen species (ROS) contribute to calpain activation and are closely associated with neuronal death. I subsequently focused on characterizing inflammatory mediators activated in response to excitotoxic injury. Using a NOX-2 knockout mouse model, I identified a critical role for NOX-2 in driving a pro-inflammatory microglial phenotype strongly associated with excitotoxic neurodegeneration.