Dr. Ford's laboratory studies the cellular and molecular mechanisms involved in the pathophysiology of atherosclerosis and stroke. Stroke is the second leading cause of death and invalidity in western society. Our laboratory is unique in that we investigate both the vascular and neurological involvement in stroke. Ischemic stroke is accompanied by the increased synthesis of inflammatory molecules, cytokines and reactive oxygen species in neurons, glia and in the cerebral vasculature. The inflammatory response to ischemic brain injury is associated with increased infarct size and poor neurological prognosis; therefore compounds that block inflammation are potentially useful as therapies to treat cerebral ischemia. Atherosclerosis is also characterized as an inflammatory disease and is one of the major causes of stroke. If uncontrolled, the inflammatory response can result in vascular lesions, which lead to an increased risk for ischemia or stroke. Work in our laboratory is focused the role of the neuregulin-erbB signaling pathway in regulation of inflammatory responses resulting from ischemic stroke. Neuregulin-1 is a pleitrophic growth factor structurally related to epidermal growth factor (EGF). We have recently demonstrated that neuregulin-1 is neuroprotective following focal stroke in vivo. The neuroprotection was associated with an inhibition of ischemia-induced inflammatory responses. Current studies are aimed at characterizing the specific role(s) for neuregulins in ischemic stroke and neuroprotection.

My research activities focus on the identification of the cellular, molecular and genetic factors underlying these disorders. My group utilizes in vivo and in vitro model as well as high-throughput tools to scan the genome (DNA), transcriptome (RNA), and proteome (protein) to understand mechanisms associated with neural and vascular development, function and pathology. We hope that these findings can be translated into treatments for these diseases and used in the development of new drugs.