Our laboratory is interested in dissecting the mechanisms of acute cerebral ischemia and carotid artery disease and in developing neuroprotective treatments, as well as novel approaches to restore neurologic function after ischemic stroke. Stroke is the third leading cause of mortality and the leading cause of disability in the United States, and a significant fraction of ischemic strokes are caused by carotid artery atherosclerosis, which results in stenosis or thrombosis of the vessels and blocks the blood flow to the brain. 

The staff has employed several novel animal models and highly innovative techniques, with increasing collaborative relationships with Dr. Neil Granger, a Boyd Professor and Chairman of the Department of Molecular and Cellular Physiology. Dr. Granger is an internationally known expert in the study of inflammation and cardiovascular & cerebrovascular diseases. 

Using wild type, gene knockout and transgenic animal models of acute and chronic brain injury, we are investigating the immune-inflammatory mechanisms of brain-vascular injury and repair after ischemic stroke, with a focus on platelet/leukocyte activation and recruitment to inflammatory cerebral vascular endothelial cells.  Using genetically engineered bone-marrow stem cells, we are investigating the potential therapeutics with stem cell transplantation, associated with molecular, cellular, and neurochemical changes as well as recovery of neurologic function after ischemic stroke in these animal models.  

Using angioplasty techniques, we are also studying the mechanisms of  neointimal hyperplasia in carotid artery stenosis under clinically relevant conditions of atherosclerosis, hypercholesterolemia, and diabetes. Angioplasty and stent placement has become the first choice of treatment for heart attack with narrowed coronary artery, and is also increasingly used for treatment of ischemic stroke with carotid artery stenosis.