Background Cerebral ischemia is a potent modulator of gene expression.
Immediate early genes undergo rapid induction after both, global and
focal cerebral ischemia. Many immediate early genes code for transcrip
tion factors. Additional genes, including those encoding for neurotrop
hic factors and neurotransmitter systems, are induced in a delayed fas
hion after cerebral ischemia. The functional significance of early and
late gene regulation after cerebral ischemia requires futher investig
ation. These changes may be beneficial (friend) or detrimental (foe).
Many of the genes are likely neuroprotective and important for recover
y, but others may be involved in ischemic cell death mediated by apopt
osis. Summary of Review We review evidence that supports the hypothesi
s that cell death after cerebral ischemia occurs through the dual path
ways of ischemic necrosis and apoptosis. Conclusions Gene regulation,
including immediate early genes, is required for programmed neuronal d
eath after trophic factor deprivation and is predicted to be involved
in apoptosis triggered by cerebral ischemia. Novel therapies following
cerebral ischemia may be directed at genes mediating either recovery
or apoptosis.