期刊
EXPERIMENTAL NEUROLOGY
卷 224, 期 1, 页码 37-47出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2010.03.021
关键词
Cannabinoid; Anandamide; 2-Arachidonoylglycerol; Neuroprotection; Neurodegeneration
资金
- European Union [MTKD-CT-2006-039039]
- Swedish Research Council [12158]
- Medical Faculty, Umea University
There is now a large volume of data indicating that compounds activating cannabinoid CBI receptors, either directly or indirectly by preventing the breakdown of endogenous cannabinoids, can protect against neuronal damage produced by a variety of neuronal insults. Given that such neurodegenerative stimuli result in increased endocannabinoid levels and that animals with genetic deletions of CB1 receptors are more susceptible to the deleterious effects of such stimuli, a case can be made for an endogenous neuroprotective role of endocannabinoids. However, this is an oversimplification of the current literature, since (a) compounds released together with the endocannabinoids can contribute to the neuroprotective effect; (b) other proteins, such as TASK-1 and PPAR alpha, are involved; (c) the CB, receptor antagonist/inverse agonist rimonabant has also been reported to have neuroprotective properties in a number of animal models of neurodegenerative disorders. Furthermore, the CB2 receptor located on peripheral immune cells and activated microglia are potential targets for novel therapies. In terms of the clinical usefulness of targeting the endocannabinoid system for the treatment of neurodegenerative disorders, data are emerging, but important factors to be considered are windows of opportunity (for acute situations such as trauma and ischemia) and the functionality of the target receptors (for chronic neurodegenerative disorders such as Alzheimer's disease). (C) 2010 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据