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首页> 外文期刊>Journal of Molecular Biology >Evidence from ITIR-FCS Diffusion Studies that the Amyloid-Beta (A beta) Peptide Does Not Perturb Plasma Membrane Fluidity in Neuronal Cells
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Evidence from ITIR-FCS Diffusion Studies that the Amyloid-Beta (A beta) Peptide Does Not Perturb Plasma Membrane Fluidity in Neuronal Cells

机译：来自ITIR-FCS扩散研究的证据，即淀粉样蛋白β（β）肽在神经元细胞中不具有扰动血浆膜流动性

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The amyloid-beta (A beta) peptide, commonly found in elevated levels in the brains of patients with Alzheimer's disease (AD) and in the cerebrospinal fluid of individuals presenting mild cognitive impairment, is thought to be one of the major factors resulting in the onset of AD. Although observed and studied at the molecular level for several decades, the exact disease pathology of AD is still not totally clear. One way in which A beta is thought to affect neurons is by influencing cell membrane fluidity, which could result in abnormal synaptic or signaling function. The effects of A beta on the fluidity of biological membranes have been studied using numerous membrane models such as artificial lipid bilayers and vesicles, living cells and membranes extracted from animal models of AD, yet there is still no consensus as to what effects A beta has, if any, on membrane fluidity. As one of the most precise and accurate means of assaying membrane dynamics, we have thus chosen fluorescence correlation spectroscopy to investigate the issue, using fluorescent membrane-targeted probes on living cells treated with A beta(1-42) oligomers and observing possible changes in membrane diffusion. Effects of A beta on viability in different cell types varied from no detectable effect to extensive cell death by 72 h post-exposure. However, there was no change in the fluidity of either ordered membrane domains or the bulk membrane in any of these cells within this period. Our conclusion from these results is that perturbation of membrane fluidity is not likely to be a factor in acute A beta-induced cytotoxicity. (C) 2018 Elsevier Ltd. All rights reserved.
机译：淀粉样蛋白β（β）肽，通常在患有轻度认知障碍的个人患者和个人脑脊液中升高的升高水平，被认为是导致的主要因素之一广告发作。虽然在分子水平观察和研究了几十年的情况下，但AD的确切疾病病理仍然没有完全清楚。 β被认为影响神经元的一种方法是通过影响细胞膜流动性，这可能导致突触异常或信号传导功能。使用诸如人工脂双层和囊泡的许多膜模型研究了β对生物膜流动性的影响，生物细胞和从广告的动物模型中提取的活细胞和膜，但仍然没有达成β有什么影响的共识，如果有的话，在膜流动性上。作为测定膜动力学的最精确和准确的方法之一，我们选择了荧光相关光谱，以研究用β（1-42）低聚物治疗的活细胞上的荧光膜靶向探针并观察可能的变化膜扩散。 β对不同细胞类型中的活力的影响因暴露后72小时没有对广泛的细胞死亡的无可检测效果不同。然而，在此期间内任何这些细胞中有序膜结构域或散装膜的流动性没有变化。我们从这些结果的结论是膜流动性的扰动不太可能是急性β诱导的细胞毒性的因素。 （c）2018年elestvier有限公司保留所有权利。

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