Michael Moskowitz, M.D.
Physician Investigator (NonCl)
Radiology, Mass General Research Institute
Professor of Neurology
Harvard Medical School
149 13th Street
Charlestown, MA 02129
|MD Tufts University School of Medicine 1968|
Dr. Moskowitz received his M.D. from Tufts University, Boston. Following postdoctoral training at the Massachusetts Institute of Technology, Cambridge, he came to the MGH in 1975 where he is currently professor of Neurology.
The Moskowitz laboratory has a long-standing interest in mechanisms regulating cerebral blood vessel function with a particular focus on interactions between neurons, glial and vascular cells. Such studies are relevant to the pathophysiology of stroke, migraine, and traumatic brain injury. In the past, his laboratory discovered the sensory innervation to the Circle of Willis and the triggering of the trigeminovascular innervation by intense neuronal and glial activity.
His laboratory also was the first to identify the neuronal 5HT receptor subtypes for abortive anti-migraine drugs. More recent research projects relate to matrix metalloproteases (MMPs) and their upregulation on vascular permeability following cortical spreading depression. In addition to MMPs, his laboratory has a long-standing interest in tissue mediators of brain injury including nitric oxide and has studied its Janus effect on vascular function and cell death.
For this project, his laboratory developed unique expertise in physiological monitoring in genetically engineered mice including techniques to evaluate cerebrovascular physiology in fully instrumented animals. His laboratory used these methods to examine the relevance of specific cell types and pathways important in cerebral ischemia such as the contribution of the endothelium and brain parenchyma to stroke protection by NO and the statins. Experiments over the past decade have examined caspases as mediators of cell demise and the role of death receptors in ischemic brain injury.
His laboratory is now examining the molecular consequences of cortical spreading depression as a potential mechanism to understand drug activity and as mechanism linking the pathophysiologic relationship between migraine and stroke.