Lynch Marina A
Trinity College Institute of Neuroscience, Trinity College, Dublin 2 Ireland.
Brain Res. 2015 Sep 24;1621:197-204. doi: 10.1016/j.brainres.2014.08.040. Epub 2014 Sep 2.
In recent years it has become clear that neuroinflammatory changes develop in the brain with age and that similar, though more profound changes, occur in neurodegenerative conditions and in animal models of neurodegeneration. These changes are linked with deterioration in plasticity and the evidence suggests that a key causative factor is microglial activation and the associated increase in production and release of inflammatory cytokines. Several groups have reported that interleukin (IL)-1β negatively impacts on hippocampal-dependent learning and has an inhibitory effect on LTP although this is concentration-dependent. Similarly other inflammatory cytokines, which are also produced by microglia similarly decrease LTP. The evidence supporting these findings will be reviewed here and will be discussed in the context of considering mechanisms by which the negative impact of neuroinflammation can be ameliorated. This article is part of a Special Issue entitled SI: Brain and Memory.
近年来，越来越清楚的是，随着年龄的增长，大脑中会出现神经炎症变化，并且在神经退行性疾病和神经退行性变的动物模型中也会发生类似但更深刻的变化。这些变化与可塑性的下降有关，证据表明一个关键的致病因素是小胶质细胞的激活以及炎症细胞因子产生和释放的相关增加。几个研究小组报告说，白细胞介素（IL）-1β对海马依赖性学习有负面影响，并且对长时程增强（LTP）有抑制作用，尽管这是浓度依赖性的。同样，其他也由小胶质细胞产生的炎症细胞因子也会类似地降低LTP。支持这些发现的证据将在此进行综述，并将在考虑改善神经炎症负面影响的机制的背景下进行讨论。本文是名为“SI：大脑与记忆”的特刊的一部分。
