APOPTOTIC NEURONAL DEATH FOLLOWING CEREBRAL-ISCHEMIA

Citation
An. Miles et Nw. Knuckey, APOPTOTIC NEURONAL DEATH FOLLOWING CEREBRAL-ISCHEMIA, Journal of clinical neuroscience, 5(2), 1998, pp. 125-145
Citations number
292
Categorie Soggetti
Neurosciences,"Clinical Neurology
ISSN journal
09675868
Volume
5
Issue
2
Year of publication
1998
Pages
125 - 145
Database
ISI
SICI code
0967-5868(1998)5:2<125:ANDFC>2.0.ZU;2-7
Abstract
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.