期刊
NEUROSCIENCE LETTERS
卷 506, 期 1, 页码 94-99出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.10.056
关键词
Alzheimer's disease; TgCRND8 mouse model; Neuroinflammation; Apoptosis; Cortical gliogenesis
资金
- Ministero dell'Istruzione, dell'Universita e della Ricerca [PRIN2008R25HBW_01]
- Ente Cassa di Risparmio di Firenze
- Universita degli Studi di Firenze, Italy
The purpose of this study was to investigate the microglia-driven apoptosis and the A beta deposits triggered generation of new microglial cells in the neocortex of TgCRND8 mice. Three- and seven-month-old TgCRND8 mice, displaying an early and widespread amyloid deposition, respectively, were used. In 7-month-old TgCRND8 mice the A beta-associated glial reaction was accompanied by an intense immunoreactivity of both TNF-alpha and inducible nitric oxide synthase, increased immunoreactivity of the pro-apoptotic protein Bax and a decrease in levels of the anti-apoptotic protein Bcl-2.Cortical and hippocampal neurons of TgCRND8 mice displayed higher immunoreactivity and higher nuclear expression of the transcription factor NF-kB than controls. It is possible that such an increase could represent a defence/compensatory response to degeneration. These findings indicate that A beta deposits activate brain-resident microglia population and astrocytes, and induce overproduction of inflammatory mediators that enhance pro- and anti-apoptotic cascades. In both 3- and 7-month-old TgCRND8 mice apparent gliogenesis was present in the vicinity of A beta plaques in the neocortex, indicating that microglia have a high proliferative rate which might play a more complex role than previously acknowledge. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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