Our Focus
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Cell death in the CNS has several unique features stemming from special characteristics of excitable cells. Our studies aim to identify regulated metabolic pathways that influence cell death in the CNS during excitotoxicity and inflammation. A particular focus is the coupling between neuronal glutamate receptors and neuronal NOX2, which generates superoxide under both normal and pathological conditions. We propose that NOX2 activity is required for normal brain plasticity, but leads to cell death during sustained activation of glutamate receptors. NOX2 is also one of several enzymes upregulated by brain microglia after injury. In a separate set of studies we are testing the possibility that suppression of this inflammatory response for a limited time interval after stroke or brain trauma can improve long-term outcomes. These studies employ novel ways of suppressing brain inflammation, including inhibitors of poly(ADP-ribose) polymerase and dietary interventions that alter the cytosolic NAD/NADH ratio.
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Lab Collaborations
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Lab PI
Jee-Yin Ahn Chris Chang Carole Escartin Tiina M. Kauppinen Jialing Liu Stephen M. Massa Kenneth L. Monson Roger Nicoll S. Scott Panter Sang Won Suh Jan Vijg Midori Yenari |
Location
Sungkyunkwan University, Suwon, Korea University of California, Berkeley CNRS and MIRCen Institute, Paris, France University of Manitoba, Winnepeg, Canada University of California, San Francisco/SFVAMC University of California, San Francisco/SFVAMC University of Utah, Salt Lake City, Utah University of California, San Francisco University of California, San Francisco/SFVAMC Hallym University, Chuncheon, Korea Albert Einstein University, New York City, NY University of California, San Francisco/SFVAMC |