Stroke affects over ¾ of a million people per year in the USA, and there is an extremely high stroke burden in the South Eastern US. People who survive stroke place a high financial and emotional burden on families and health care systems. To date there are no currently approved therapies to reduce brain injury following stroke. Recent clinical trials based on blocking acute excitotoxicity (mediated by glutamate and free radicals) have been disappointing.
An alternative approach is to investigate endogenous protection via mechanisms of induced tolerance. Cells organs and whole organisms can acquire tolerance to normally harmful stressor, if they are pre-exposed to a mild sub toxic dose of that stressor (preconditioning). Ischemic tolerance is the phenomenon whereby prior exposure to brief non-harmful ischemia results in tolerance to subsequent exposure to typically harmful ischemia (perhaps the ultimate expression of “what does not kill you makes you stronger!!!”).
While a number of features have been reported, such as the role of new protein synthesis and various signal transduction mechanisms blocking cell death signaling, we still have little understanding of how the preconditioning event actually results in the protected phenotype. My research focuses on molecular mechanisms regulating endogenous neuroprotection.
Lab Members Robert Meller, D.Phil.
Andrea Pearson, BA
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