Astrocytes: Conductors of the Alzheimer disease neuroinflammatory symphony

被引:191
作者
Medeiros, Rodrigo [1 ]
LaFerla, Frank M. [1 ]
机构
[1] Univ Calif Irvine, Dept Neurobiol & Behav, Inst Memory Impairments & Neurol Disorders, Irvine, CA 92697 USA
关键词
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; NEURONAL CYCLOOXYGENASE-2 EXPRESSION; LONG-TERM POTENTIATION; TNF-ALPHA; A-BETA; TRANSGENIC INHIBITION; MICROGLIAL ACTIVATION; HIPPOCAMPAL-FORMATION;
D O I
10.1016/j.expneurol.2012.10.007
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alzheimer disease (AD) is the most prevalent cause of dementia in humans, and the symptoms are commonly manifested after the seventh decade of life. Numerous pathological changes have been described in the post-mortem brains of AD patients, including senile plaques, neurofibrillary tangles, neuroinflammation, synapse loss, and neuronal death. Reactive astrocytes surrounding senile plaques seem to be responsible for the on-going inflammatory process in the disease through the release of cytokines and other toxic products. However, little is known about the regulation of these cells in the AD brain. Here we discuss the potential translational impact of the recent findings of Carrero and colleagues, published in Experimental Neurology, that shows the underlying molecular mechanism of astrocyte activation in response to beta-amyloid (A beta). Like-wise, the relevance of pro-inflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin-beta (IL-1 beta), cyclooxygenase-2 (COX-2) and nuclear factor-kappa B (NF-kappa B), as integral players in disease progression will be discussed. (c) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:133 / 138
页数:6
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