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阿尔茨海默病中的膜生物物理学和力学。

Membrane biophysics and mechanics in Alzheimer's disease.

机构信息

Department of Biological Engineering, University of Missouri, 240 Agricultural Engineering Building, Columbia, MO 65211, USA.

出版信息

Mol Neurobiol. 2010 Jun;41(2-3):138-48. doi: 10.1007/s12035-010-8121-9. Epub 2010 May 1.

DOI:10.1007/s12035-010-8121-9
PMID:20437210
Abstract

Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-beta peptide (Abeta), a major component of senile plaques, has been shown to exert multiple toxic effects to neurons, astrocytes, glial cells, and brain endothelium. Oligomeric Abeta can disturb the structure and function of cell membranes and alter membrane mechanical properties, such as membrane fluidity and molecular order. Much of these effects are attributed to their capability to trigger oxidative stress and inflammation. In this review, we discuss the effects of Abeta on neuronal cells, astrocytes, and cerebral endothelial cells with special emphasis on cell membrane properties and cell functions.

摘要

阿尔茨海默病是一种慢性神经退行性疾病,其特征是神经元丧失、脑血管炎症以及脑实质和脑血管中老年斑的积累。淀粉样β肽(Abeta)是老年斑的主要成分,已被证明对神经元、星形胶质细胞、神经胶质细胞和脑内皮细胞具有多种毒性作用。寡聚 Abeta 可扰乱细胞膜的结构和功能,并改变膜的机械特性,如膜流动性和分子有序性。这些影响的大部分归因于它们引发氧化应激和炎症的能力。在这篇综述中,我们讨论了 Abeta 对神经元细胞、星形胶质细胞和脑内皮细胞的影响,特别强调了细胞膜特性和细胞功能。

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Membrane biophysics and mechanics in Alzheimer's disease.阿尔茨海默病中的膜生物物理学和力学。
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本文引用的文献

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Lipid rafts as a membrane-organizing principle.脂筏作为一种膜组织原则。
Science. 2010 Jan 1;327(5961):46-50. doi: 10.1126/science.1174621.
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Secretory phospholipase A2 type III enhances alpha-secretase-dependent amyloid precursor protein processing through alterations in membrane fluidity.分泌型磷脂酶 A2 同工酶 III 通过改变膜流动性增强 α-分泌酶依赖性淀粉样前体蛋白的加工。
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Alzheimer's Disease as a Membrane Disorder: Spatial Cross-Talk Among Beta-Amyloid Peptides, Nicotinic Acetylcholine Receptors and Lipid Rafts.作为一种膜紊乱疾病的阿尔茨海默病:β-淀粉样肽、烟碱型乙酰胆碱受体与脂筏之间的空间相互作用
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APP/Aβ structural diversity and Alzheimer's disease pathogenesis.淀粉样蛋白前体蛋白/β 结构多样性与阿尔茨海默病发病机制。
Neurochem Int. 2017 Nov;110:1-13. doi: 10.1016/j.neuint.2017.08.007. Epub 2017 Aug 12.
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Endogenously generated amyloid-β increases stiffness in human neuroblastoma cells.内源性生成的β-淀粉样蛋白会增加人神经母细胞瘤细胞的硬度。
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Amyloid beta oligomers induce neuronal elasticity changes in age-dependent manner: a force spectroscopy study on living hippocampal neurons.淀粉样β寡聚体以年龄依赖性方式诱导神经元弹性变化:对活体海马神经元的力谱研究
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Signaling pathways regulating neuron-glia interaction and their implications in Alzheimer's disease.调节神经元-胶质细胞相互作用的信号通路及其在阿尔茨海默病中的意义。
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Soluble aggregates of the amyloid-beta peptide are trapped by serum albumin to enhance amyloid-beta activation of endothelial cells.淀粉样β肽的可溶性聚集物被血清白蛋白捕获,以增强淀粉样β肽对血管内皮细胞的激活作用。
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NAD(P)H oxidase-mediated reactive oxygen species production alters astrocyte membrane molecular order via phospholipase A2.NAD(P)H氧化酶介导的活性氧生成通过磷脂酶A2改变星形胶质细胞膜分子有序性。
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The interaction of beta-amyloid protein with cellular membranes stimulates its own production.β-淀粉样蛋白与细胞膜的相互作用会刺激其自身的产生。
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Increased membrane cholesterol might render mature hippocampal neurons more susceptible to beta-amyloid-induced calpain activation and tau toxicity.膜胆固醇增加可能使成熟海马神经元更容易受到β-淀粉样蛋白诱导的钙蛋白酶激活和tau蛋白毒性的影响。
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Neurovascular mechanisms and blood-brain barrier disorder in Alzheimer's disease.阿尔茨海默病中的神经血管机制与血脑屏障紊乱
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Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer's brain is mediated by the JNK-AP1 signaling pathway.β-淀粉样肽在人脑血管内皮细胞和阿尔茨海默病大脑中诱导的炎症基因表达是由JNK-AP1信号通路介导的。
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Altered Ca2+ dependence of synaptosomal plasma membrane Ca2+-ATPase in human brain affected by Alzheimer's disease.阿尔茨海默病影响的人脑突触体细胞膜钙-ATP酶钙依赖性的改变。
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