Richard S. Morrison

yael@u.washington.edu
Professor, Department of Neurological Surgery

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The primary objective of our research is to characterize signal transduction pathways associated with neuronal cell death in the central nervous system, the specific circumstances (injury and disease) that activate them and the mechanisms by which they promote declining viability. Specific studies are currently focused on the p53 gene. The tumor suppressor gene, p53, a key regulator of cellular proliferation, has recently been associated with the induction of cell death in response to some forms of cellular damage. Although the function of this gene has been studied primarily within the context of oncological issues, a possible role for p53-related modulation of neuronal viability has been suggested by the finding that p53 expression is increased in damaged neurons in models of ischemia and epilepsy. We are pursuing the possibility that p53 induction initiates or participates in an intracellular pathway that culminates in neuronal cell death. In order to accomplish this goal we are:

1. Evaluating the biochemical pathways that regulate p53 expression and p53 transcriptional activity in central nervous system neurons;
2. Evaluating the potential mechanisms by which p53 promotes irreversible neuronal cell injury, including analysis of Bcl-2 and caspase family members.

Differential display and cDNA array technology are being used to identify unique genes regulated by p53 in injured neurons. Elucidating the function of p53 in the nervous system may shed light on the regulation of neuronal survival and activity in response to injury and neurological disease.