My laboratory studies the roles of microglial-mediated inflammatory responses in health and disease using in vitro and in vivo methodologies. For the former, we use electrophysiology, calcium imaging and molecular biology to examine effects of stimuli such as amyloid-beta peptide on microglial functional responses. For the latter, immunohistochemical analysis is applied to characterize the mechanisms by which activated microglia cause perturbations to blood brain barrier and alter neuronal viability in animal models of Alzheimer’s and other neurodegenerative diseases. We are also interested in pharmacological modulation of microglial responses as a strategy for neuroprotection in diseased brain.
Combined minocycline plus pyruvate treatment enhances effects of each agent to inhibit inflammation, oxidative damage, and neuronal loss in an excitotoxic animal model of huntington's disease. Neuroscience. 2006 Jun 27
Mitochondrial ligand inhibits store-operated calcium influx and COX-2 production in human microglia.J Neurosci Res. 2006 May 15;83(7):1293-8.
Minocycline or iNOS inhibition block 3-nitrotyrosine increases and blood-brain barrier leakiness in amyloid beta-peptide-injected rat hippocampus.
Exp Neurol. 2006 Apr;198(2):552-7