Caspase-3-mediated cleavage of PHF-1 tau during apoptosis irrespective of excitotoxicity and oxidative stress: an implication to Alzheimer's disease
- Authors
- Kang, Hyo Jung; Yoon, Won Joo; Moon, Gyeong Joon; Kim, Doo Yeon; Sohn, Seonghyang; Kwon, Hyuk Jae; Gwag, Byoung Joo
- Issue Date
- Apr-2005
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Alzheimer's disease; neurofibrillary tangles; caspase-3; apoptosis; tau; glutamate
- Citation
- NEUROBIOLOGY OF DISEASE, v.18, no.3, pp 450 - 458
- Pages
- 9
- Journal Title
- NEUROBIOLOGY OF DISEASE
- Volume
- 18
- Number
- 3
- Start Page
- 450
- End Page
- 458
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/36700
- DOI
- 10.1016/j.nbd.2004.12.004
- ISSN
- 0969-9961
1095-953X
- Abstract
- Excitotoxicity, oxidative stress, and apoptosis have been recognized as routes to neuronal death in various neurological diseases. We examined the possibility that PHF-1 tau, a substrate for various proteases, would be selectively cleaved depending upon routes of neuronal death. Cleavage form of PHF-1 tau was not observed in cortical cell cultures exposed to excitotoxins or oxidative stress that cause neuronal cell necrosis. PHF-1 tau was cleaved within 8 h following exposure of cortical cell cultures to apoptosis-inducing agents. This cleavage was blocked by inclusion of zDEVD-fmk, an inhibitor of caspase-3, and accompanied by activation of caspase-3. Levels and cleavage of PHF-1 tau were markedly increased in AD brain compared with control. Moreover, PHF-1 tau and active caspase-3 were colocalized mostly in tangle-bearing neurons. The current findings suggest that PHF-1 tau is cleaved by caspase-3 during apoptosis and neurodegenerative process in AD. (c) 2005 Elsevier Inc. All rights reserved.
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