Heads of Laboratories
One approach for gaining insight into the complex mammalian nervous system is to study diseases that perturb its function at the molecular level. Such studies can reveal the roles of critical molecules by identifying those that, by their alteration or absence, cause disease. Dr. Strickland’s lab investigates mouse models of neurological diseases, using genetic, cell biological and biochemical approaches to investigate neurovascular function, dysfunction and repair.
Neurological disorders of the central nervous system represent profound medical problems worldwide. Alzheimer’s disease and stroke affect millions of people and have severe physical, psychological and financial consequences. By using mouse models of neurological diseases, Dr. Strickland is working to elucidate the molecular mechanisms by which neural function is disrupted.
In investigating neurovascular dysfunction, the Strickland lab maintains two general lines of study: the mechanisms underlying the pathogenesis of Alzheimer’s disease and intracerebral hemorrhagic stroke. Cerebrovascular defects contribute to the progression of Alzheimer’s pathology, and members of the lab are using transgenic mouse models of Alzheimer’s to evaluate blood brain barrier damage and the roles that blood clot formation and degradation play in this disease. Their research has determined that the amyloid-β peptide, which is considered to be a causative factor in Alzheimer’s, interacts with fibrinogen to promote fibrin accumulation in the brain and increase brain inflammation. This peptide also alters blood clot structure and clot degradation, which could compromise blood flow, exacerbate inflammation and lead to neuronal death. These results suggest that fibrin and the mechanisms involved in its accumulation and clearance may present novel therapeutic targets for slowing progression of Alzheimer’s disease.
Cellular and molecular defects in the cerebral vasculature can also lead to intracerebral hemorrhage, the most devastating type of stroke due to its high rates of death and disability. Members of the Strickland lab have generated a conditional knockout mouse model of spontaneous hemorrhagic stroke to analyze the role of astrocytic laminin in cerebrovascular integrity and brain vascular smooth muscle cell differentiation. Their results suggest that astrocytic laminin may be a novel target for treatment and prevention of hemorrhagic stroke in humans.
Dr. Strickland received his bachelor’s degree in chemistry from Rhodes College in Memphis in 1968 and his Ph.D. in biochemistry from the University of Michigan in 1972. He came to Rockefeller in 1973 as a research associate and was named assistant professor in 1975 and associate professor in 1980. He moved to Stony Brook University in 1983 as an associate professor and was promoted to professor in 1987. He returned to Rockefeller in 2000 as head of the Laboratory of Neurobiology and Genetics and dean of graduate and postgraduate studies.
Dr. Strickland received an honorary doctor of science degree in 2006 from Rhodes College, a Distinguished Alumni Award in 2002 and a Distinguished Graduate Award from the University of Michigan in 2001. He was named a John Simon Guggenheim Memorial Foundation Fellow in 1998 and was an established investigator for the American Heart Association from 1981 to 1986. He received a Jane Coffin Childs Postdoctoral Fellowship in 1973 and a National Science Foundation Graduate Research Fellowship in 1970. In 2006, together with his daughter, Eliza Strickland, he published The Illustrated Timeline of Science: A Crash Course in Words and Pictures.
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