Heads of Laboratories
Vice President for Educational Affairs and Dean of Graduate and Post Graduate Studies
Research Professor
Laboratory of Neurobiology and Genetics
neurogenlab@rockefeller.edu
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 neurological function, dysfunction and repair.
Neurological disorders of the central nervous system represent profound medical problems worldwide. Alzheimer’s disease, Parkinson’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 neuronal dysfunction, the Strickland lab maintains two general lines of study: the mechanisms underlying
Alzheimer’s disease pathogenesis and neurodegeneration caused by excitotoxicity. 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 peptide, which is considered to be a causative factor in Alzheimer’s, promotes fibrin accumulation in the brain and
increases brain inflammation. This peptide also alters blood clot formation and degradation, which can 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 the disease.
Stroke, seizures and alcohol abuse can lead to excitotoxic neuronal death. Their recently published work suggests that tissue plasminogen activator and its inhibitor, PAI-1, may be the determining factors of cell death or survival after alcohol exposure to the fetal brain. Furthermore, the kainate receptor subunit KA1 is of particular interest as it is involved in excitotoxicity. Currently, members of the lab are using KA1 knockout mice to study the role of KA1 in excitotoxic neurodegeneration in the hippocampus and its impact on mouse behavior. These animals show signs of neuroprotection, which may provide a novel therapeutic approach to the treatment of stroke.
CAREER
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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