Inflammatory factors are elevated in brain microvessels in Alzheimer's disease
Inflammatory factors are elevated in brain microvessels in Alzheimer's disease
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DOI：
10.1016/s0197-4580(01)00276-7
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发表时间：
2001-11-01
影响因子：
4.2
通讯作者：
Ovase, R
中科院分区：
文献类型：
--
作者：
Grammas, P;Ovase, R
在阿尔茨海默病（AD）中，炎症过程发生在病理易感的大脑区域。本研究的目的是比较从AD患者的大脑中分离的血管与对照大脑的微血管中微血管相关细胞因子的释放和存在。从AD患者和年龄匹配的对照中分离出微血管，没有神经退行性疾病的证据。介质中的炎症因子通过ELISA定量，微血管相关介质通过Western blot评估。我们的研究结果表明，与非阿尔茨海默病微血管相比，未受刺激的阿尔茨海默病微血管释放的白细胞介素-1 β -(IL-1 β)、IL-6和肿瘤坏死因子α (tnf - α)水平明显更高。微血管相关单核细胞化学引诱蛋白（MCP-1）和IL-10水平在ad衍生的微血管中较高，但在非ad微血管中未检测到。这些结果表明，大脑微循环向AD脑环境提供炎症介质，并可能参与该疾病神经元损伤和死亡的发病机制。(C) 2001爱思唯尔科学公司版权所有。
In Alzheimer's disease (AD) inflammatory processes occur in pathologically vulnerable brain regions. The objective of this study is to compare both the release and the presence of microvessel-associated cytokines in vessels isolated from the brains of AD patients to microvessels from control brains. Microvessels are isolated from the cortices of AD patients and age-matched controls, without evidence of neurodegenerative disease. Inflammatory factors in the media are quantitated by ELISA and microvessel-associated mediators assessed by Western blot. Our results demonstrate that unstimulated AD microvessels release significantly higher levels of interleukin-1 beta-(IL-1 beta), IL-6, and tumor necrosis factor alpha (TNF-alpha) compared to non-AD microvessels. Levels of microvessel-associated monocyte chemoattractant protein (MCP-1) and IL-10 are high in AD-derived microvessels, but not detectable in non-AD microvessels. These results suggest that the cerebral microcirculation contributes inflammatory mediators to the milieu of the AD brain and may be involved in the pathogenesis of neuronal injury and death in this disorder. (C) 2001 Elsevier Science Inc. All rights reserved.