Assessment of activation of the plasma kallikrein-kinin system in frontal and temporal cortex in Alzheimer's disease and vascular dementia
Assessment of activation of the plasma kallikrein-kinin system in frontal and temporal cortex in Alzheimer's disease and vascular dementia
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DOI：
10.1016/j.neurobiolaging.2010.09.024
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发表时间：
2012-07-01
影响因子：
4.2
通讯作者：
Kehoe, Patrick G.
中科院分区：
文献类型：
--
作者：
Ashby, Emma L.;Love, Seth;Kehoe, Patrick G.
脑血流量减少和血脑屏障破坏是阿尔茨海默病（AD）的特征。血浆激肽释放酶-激肽系统通过释放血管活性缓激肽（BK）调节脑血管紧张度。脑室内输注A β 1-40可增强BK释放，这表明该系统的活性可能在AD中升高。我们研究了该系统的激活蛋白酶，血浆激肽释放酶（PK），在额叶和颞叶脑组织的尸检确诊病例AD，血管性痴呆（VaD），和控制的配置文件。神经元特异性烯醇化酶信使核糖核酸（mRNA）和蛋白质的测量用于调整神经元损失。AD患者的额叶皮质和VaD患者的额叶和颞叶皮质中校正PK mRNA显著增加。在AD和VaD中观察到PK蛋白水平的相似趋势。AD患者额叶和颞叶皮质PK活性显著升高。AD中PK活性增加可能导致BK释放增加，从而可能影响脑血流量和血管通透性。(C)2012 Elsevier Inc. All rights reserved.
Decreased cerebral blood flow and blood-brain barrier disruption are features of Alzheimer's disease (AD). The plasma kallikrein-kinin system modulates cerebrovascular tone through release of vasoactive bradykinin (BK). Cerebroventricular infusion of A beta 1-40 enhances BK release, suggesting that the activity of this system may be elevated in AD. We investigated the profile of the activating protease of this system, plasma kallikrein (PK), in frontal and temporal brain tissue from postmortem confirmed cases of AD, vascular dementia (VaD), and controls. Measurements of neuron specific enolase messenger ribonucleic acid (mRNA) and protein were used to adjust for neuronal loss. Adjusted PK mRNA was significantly increased in the frontal cortex in AD, and the frontal and temporal cortex in VaD. Similar trends were seen for PK protein level in AD and VaD. PK activity was significantly increased in the frontal and temporal cortex in AD. Increased PK activity in AD is likely to contribute to increased BK release and may thereby influence cerebral blood flow and vascular permeability. (C) 2012 Elsevier Inc. All rights reserved.