期刊
NEUROBIOLOGY OF AGING
卷 36, 期 2, 页码 710-719出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2014.09.019
关键词
Alzheimer's disease; CB2; CCL2; Endocannabinoid system; Microglia; Neuroinflammation
资金
- Deutsche Forschungsgemeinschaft (DFG) [FOR926 SP10, FOR926 SP6, CP2]
Several studies have indicated that the cannabinoid receptor 2 (CB2) plays an important role in neuroinflammation associated with Alzheimer's disease (AD) progression. The present study examined the role of CB2 in microglia activation in vitro as well as characterizing the neuroinflammatory process in a transgenic mouse model of AD (APP/PS1 mice). We demonstrate that microglia harvested from CB2(-/-) mice were less responsive to pro-inflammatory stimuli than CB2(+/+) microglia, based on the cell surface expression of ICAM and CD40 and the release of chemokines and cytokines CCL2, IL-6, and TNF alpha. Transgenic APP/PS1 mice lacking CB2 showed reduced percentages of microglia and infiltrating macrophages. Furthermore, they showed lowered expression levels of pro-inflammatory chemokines and cytokines in the brain, as well as diminished concentrations of soluble A beta 40/42. The reduction in neuroinflammation did not affect spatial learning and memory in APP/PS1*CB2(-/-) mice. These data suggest a role for the CB2 in Alzheimer's disease-associated neuroinflammation, independent of influencing Ab-mediated pathology and cognitive impairment. (C) 2015 Elsevier Inc. All rights reserved.
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