Transient cerebral ischaemia accompanies a number of disease processes
, including stroke, subarachnoid haemorrhage and head injury, that hav
e a profound social and economic impact on our community. The developm
ent of neuroprotective agents that reduce the morbidity associated wit
h these diverse conditions requires an understanding of the mechanisms
of neuronal death following cerebral ischaemia. There is increasing e
vidence that a significant proportion of neurons die following ischaem
ia by a process called apoptosis. Apoptosis involves the activation of
a highly regulated series of intracellular events in which the neuron
actively participates in its own death. Genes such as bcl-2 and prote
olytic enzymes such as the caspases, which have been shown to play an
important role in apoptotic cell death in other cell types, are now be
ing investigated for their role in apoptotic neuronal death. This revi
ew will focus on current knowledge of the intracellular pathways of ap
optosis, with particular reference to their role in ischaemic neuronal
death. (C) Harcourt Brace & Co. Ltd 1998.