中国作者重要发表 - 小鼠阿尔茨默样早老蛋白-1、-2双敲除条件下氧化应激和星形胶质细胞增生的效应



小鼠阿尔茨默样早老蛋白-1、-2双敲除条件下氧化应激和星形胶质细胞增生的效应





Increased oxidative stress and astrogliosis responses in conditional double-knockout mice of Alzheimer-like presenilin-1 and presenilin-2





Zhu M., Gu F., Shi J., Hu J., Hu Y., Zhao Z. 2009/5/29 18:38:57

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Free Radical Biology and Medicine, 2008, Volume 45, Issue 10




Conditional presenilin 1 and presenilin 2 double knockout causes memory dysfunction and reproduces neurodegenerative phenotypes of Alzheimer disease (AD) in mice. Oxidative stress has been long implicated predominantly in amyloidosis-mediated AD pathologies; however, its role in response to the loss-of-function pathogenic mechanism of AD remains unclear. In this study, we examined the oxidative stress status in PS1 and PS2 double-knockout (PS cDKO) mice using F2-isoprostanes (iPF2α-III) as the marker of lipid peroxidation. Lipid peroxidation was enhanced in a gender- and age-related manner in the PS cDKO mice independent of brain Aβ deposition. Such oxidative abnormalities predominantly in cerebral cortex at 2-4 months of age preceded the onset of many pronounced AD neuropathologies, suggesting that increased lipid peroxidation is not only an early pathophysiological response to PS inactivation, but also a potential culprit responsible for the AD-like neurodegenerative pathologies in the PS cDKO mice. Western blot analysis of cortical glial fibrillary acidic protein demonstrated an increased astrogliosis response to PS inactivation, in particular in the PS cDKO mice at as young as 2 months of age, suggesting that lipid peroxidation and neuronal injury may be closely associated with the loss-of-function neuropathogenic mechanism of AD. © 2008 Elsevier Inc. All rights reserved.



Correspondence Address: Zhao, Z.; Key Laboratory of Brain Functional Genomics, Ministry of Education of China, Science and Technology Commission of Shanghai Municipality, 3663 Zhongshan Road (N), Shanghai 200062, China; email: zzhao@brain.ecnu.edu.cn



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