Implication of cysteine proteases calpain, cathepsin and caspase in ischemic neuronal death of primates

Although more than 8000 papers of apoptosis are published annually, there are very few reports concerning necrosis in the past few years. A number of recent studies using lower species animals have suggested that the cornu Ammonis (CA) 1 neuronal death after brief global cerebral ischemia occurs by...

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Bibliographic Details
Published in:Progress in neurobiology 2000-10, Vol.62 (3), p.273-295
Main Author: Yamashima, T
Format: Article
Language:English
Subjects:
Animals
Brain Ischemia - metabolism
Brain Ischemia - pathology
Brain Ischemia - physiopathology
Calpain - metabolism
Caspases - metabolism
cathepsins
Cathepsins - metabolism
Cell Death - physiology
cysteine proteinase
Hippocampus - pathology
Hippocampus - physiopathology
Hippocampus - ultrastructure
Neurons - metabolism
Neurons - pathology
Neurons - ultrastructure
Primates
Primates - anatomy & histology
Primates - metabolism
Pyramidal Cells - metabolism
Pyramidal Cells - pathology
Pyramidal Cells - ultrastructure
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Summary:Although more than 8000 papers of apoptosis are published annually, there are very few reports concerning necrosis in the past few years. A number of recent studies using lower species animals have suggested that the cornu Ammonis (CA) 1 neuronal death after brief global cerebral ischemia occurs by apoptosis, an active and genetically controlled cell suicide process. However, the studies of monkeys and humans rather support necrosis, the calpain-mediated release of lysosomal enzyme cathepsin after ischemia conceivably contributes to the cell degeneration of CA1 neurons. This paper provides an overview of recent developments in ischemic neuronal death, presents the cascade of the primate neuronal death with particular attentions to the cysteine proteases, and also indicates selective cathepsin inhibitors as a novel neuroprotectant. Furthermore, the possible interaction of calpain, cathepsin, and caspase in the cascade of ischemic neuronal death is discussed.
ISSN:0301-0082
DOI:10.1016/s0301-0082(00)00006-x