Abstract:
:Calpain activation has been implicated in the pathogenesis of Alzheimer's disease. Okadaic acid, a protein phosphatase-2A inhibitor, has been used in Alzheimer's disease research models to increase tau phosphorylation and induce neuronal death. We previously reported that okadaic acid induced predominant activation of caspase-3 in immature neurons, but less activation in mature neurons. We found here that, in okadaic-acid-treated mature neurons, levels of an inactive form of m-calpain decreased and levels of calpain-cleaved spectrin and synapsin-I fragments increased, suggestive of calpain activation. Pretreatment with calpain inhibitor decreased lactate dehydrogenase release by 20% and increased average dendritic branch length by 50% compared with neurons treated with okadaic acid alone. These findings suggest that calpain is activated during okadaic-acid-induced neurodegeneration and calpain inhibition can be protective against it.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Yoon S,Choi J,Huh JW,Hwang O,Kim Ddoi
10.1097/01.wnr.0000214398.04093.7fsubject
Has Abstractpub_date
2006-05-15 00:00:00pages
689-92issue
7eissn
0959-4965issn
1473-558Xpii
00001756-200605150-00001journal_volume
17pub_type
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