A major emphasis in our group is directed towards understanding the mechanisms of neuroprotection by ischemic preconditioning (IPC) against cerebral ischemia (as elicited by a stroke or cardiac arrest). We have demonstrated in brain that IPC is mediated by two key signaling pathways.
Another area of emphasis in our group is defining mechanisms by which some signaling pathways alter synaptic function following cardiac arrest.
A third area of emphasis in our group is the definition of the mechanisms of mitochondrial dysfunction following cerebral ischemia.