The p53 tumor suppressor gene is a sequence-specific transcription factor t
hat activates the expression of genes engaged in promoting growth arrest or
cell death in response to genotoxic stress. A possible role for p53-relate
d modulation of neuronal viability has been suggested by the finding that p
53 expression is elevated in damaged neurons in acute models of injury such
as ischemia and epilepsy and in brain tissue samples derived from patients
with chronic neurode-generative diseases. Moreover, the absence of p53 has
been shown to protect neurons from a wide variety of acute toxic insults.
Signal transduction pathways associated with p53-induced cell death are bei
ng unraveled and suggest that intervention may prove fruitful in maintainin
g neuronal viability and restoring function following cytopathic insults.