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膜界面上的淀粉样蛋白:对神经退行性变的影响。

Amyloids on Membrane Interfaces: Implications for Neurodegeneration.

机构信息

School of Biological Sciences, National Institute of Science Education and Research, Bhubaneswar, India.

Homi Bhabha National Institute, Mumbai, India.

出版信息

J Membr Biol. 2022 Dec;255(6):705-722. doi: 10.1007/s00232-022-00245-x. Epub 2022 Jun 7.

DOI:10.1007/s00232-022-00245-x
PMID:35670831
Abstract

Membrane interfaces are vital for various cellular processes, and their involvement in neurodegenerative disorders such as Alzheimer's and Parkinson's disease has taken precedence in recent years. The amyloidogenic proteins associated with neurodegenerative diseases interact with the neuronal membrane through various means, which has implications for both the onset and progression of the disease. The parameters that regulate the interaction between the membrane and the amyloids remain poorly understood. The review focuses on the various aspects of membrane interactions of amyloids, particularly amyloid-β (Aβ) peptides and Tau involved in Alzheimer's and α-synuclein involved in Parkinson's disease. The genetic, cell biological, biochemical, and biophysical studies that form the basis for our current understanding of the membrane interactions of Aβ peptides, Tau, and α-synuclein are discussed.

摘要

膜界面对于各种细胞过程至关重要,近年来,它们在阿尔茨海默病和帕金森病等神经退行性疾病中的作用已成为研究重点。与神经退行性疾病相关的淀粉样蛋白通过各种方式与神经元膜相互作用,这对疾病的发生和进展都有影响。调节膜与淀粉样蛋白相互作用的参数仍知之甚少。本综述重点讨论了淀粉样蛋白的各种膜相互作用方面,特别是与阿尔茨海默病相关的淀粉样β(Aβ)肽和 Tau,以及与帕金森病相关的α-突触核蛋白。讨论了构成我们目前对 Aβ肽、Tau 和 α-突触核蛋白与膜相互作用的理解的遗传、细胞生物学、生物化学和生物物理研究。

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本文引用的文献

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Experimentally Consistent Simulation of Aβ Peptides with a Minimal NMR Bias.具有最小核磁共振偏差的 Aβ 肽的实验一致模拟
J Phys Chem B. 2020 Sep 24;124(38):8266-8277. doi: 10.1021/acs.jpcb.0c07129. Epub 2020 Sep 9.
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Comparison of Synthetic Neuronal Model Membrane Mimics in Amyloid Aggregation at Atomic Resolution.在原子分辨率下比较淀粉样蛋白聚集的合成神经元模型膜模拟物。
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Do Lewy bodies contain alpha-synuclein fibrils? and Does it matter? A brief history and critical analysis of recent reports.
路易体是否含有α-突触核蛋白纤维?这有关系吗?对近期报告的简要历史回顾和批判性分析。
Neurobiol Dis. 2020 Jul;141:104876. doi: 10.1016/j.nbd.2020.104876. Epub 2020 Apr 25.
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Insoluble tau aggregates induce neuronal death through modification of membrane ion conductance, activation of voltage-gated calcium channels and NADPH oxidase.不溶性 tau 聚集体通过改变膜离子电导、激活电压门控钙通道和 NADPH 氧化酶诱导神经元死亡。
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Alpha-Synuclein Physiology and Pathology: A Perspective on Cellular Structures and Organelles.α-突触核蛋白的生理学与病理学:关于细胞结构和细胞器的观点
Front Neurosci. 2020 Jan 23;13:1399. doi: 10.3389/fnins.2019.01399. eCollection 2019.
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The Mitochondria-Endoplasmic Reticulum Contacts and Their Critical Role in Aging and Age-Associated Diseases.线粒体-内质网接触及其在衰老和年龄相关疾病中的关键作用。
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Membrane-mediated fibrillation and toxicity of the tau hexapeptide PHF6.tau 六肽 PHF6 的膜介导纤维形成和毒性。
J Biol Chem. 2019 Oct 18;294(42):15304-15317. doi: 10.1074/jbc.RA119.010003. Epub 2019 Aug 22.
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The physiological role of α-synuclein and its relationship to Parkinson's Disease.α-突触核蛋白的生理作用及其与帕金森病的关系。
J Neurochem. 2019 Sep;150(5):475-486. doi: 10.1111/jnc.14810. Epub 2019 Jul 28.
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The role of lipids in α-synuclein misfolding and neurotoxicity.脂质在α-突触核蛋白错误折叠和神经毒性中的作用。
J Biol Chem. 2019 Jun 7;294(23):9016-9028. doi: 10.1074/jbc.REV119.007500. Epub 2019 May 7.
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