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| October 1998, Volume 5, Number 10, Pages 823-831 |
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| Review |
| ICE, neuronal apoptosis and neurodegeneration |
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| Robert M Friedlander1 and Junying Yuan2,a |
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1Neurosurgical Service, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114 USA
2Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA
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aAuthor for correspondence: tel: 617 432-4170; fax: 617 432-4177; email: jyuan@hms.harvard.edu |
Edited by G. Melino
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| Abstract |
 | Significant progress has recently occurred in the understanding of the molecular mechanisms mediating vertebrate programmed cell death, or apoptosis. New advances in this field have stemmed from the identification of ICE (caspase-1) as the founding member of the mammalian caspase cell death family. Apoptotic cell death plays an important role in neuronal cell death. Both in vitro and in vivo evidence implicates ICE as an important factor in neuronal apoptosis, especially under pathological conditions. In addition, other caspases, such as caspase-3, have also been shown to be activated and may play a role in pathological neuronal loss. Understanding the basic mechanisms mediating cell death in neurodegenerative disease may lead to the development of novel approaches for the treatment of diseases featuring apoptosis. |
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| Keywords |
 | apoptosis; ICE; caspase; pathological cell death |
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| Received 20 March 1998; revised 18 June 1998; accepted 23 June 1998 |
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| October 1998, Volume 5, Number 10, Pages 823-831 |
| Table of contents Previous Abstract Next Article PDF |
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