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Revisiting the Impact of Neurodegenerative Proteins in Epilepsy: Focus on Alpha-Synuclein, Beta-Amyloid, and Tau.重新审视神经退行性变蛋白在癫痫中的作用:聚焦于α-突触核蛋白、β-淀粉样蛋白和tau蛋白。
Biology (Basel). 2020 Jun 12;9(6):122. doi: 10.3390/biology9060122.
2
[Expression of proteins related neurodegeneration in autopsy brains of the aged].[老年尸检大脑中与神经退行性变相关蛋白质的表达]
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Aβ, Tau, and α-Synuclein aggregation and integrated role of PARK2 in the regulation and clearance of toxic peptides.β-淀粉样蛋白、Tau 蛋白和 α-突触核蛋白聚集以及 PARK2 在调节和清除毒性肽中的综合作用。
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4
Endogenous Murine Amyloid-β Peptide Assembles into Aggregates in the Aged C57BL/6J Mouse Suggesting These Animals as a Model to Study Pathogenesis of Amyloid-β Plaque Formation.内源性小鼠β-淀粉样肽在老年C57BL/6J小鼠中聚集成聚集体,表明这些动物可作为研究β-淀粉样斑块形成发病机制的模型。
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Cerebrospinal Fluid and Plasma Biomarkers in Neurodegenerative Diseases.神经退行性疾病中的脑脊液和血浆生物标志物。
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Potential Diagnostic Value of Red Blood Cells α-Synuclein Heteroaggregates in Alzheimer's Disease.红细胞α-突触核蛋白杂合体在阿尔茨海默病中的潜在诊断价值。
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Is alpha-synuclein pathology a target for treatment of neurodegenerative disorders?α-突触核蛋白病变是神经退行性疾病的治疗靶点吗?
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Small-molecule PET Tracers for Imaging Proteinopathies.小分子 PET 示踪剂用于成像蛋白病。
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本文引用的文献

1
Neurodegenerative pathways as targets for acquired epilepsy therapy development.作为获得性癫痫治疗开发靶点的神经退行性通路
Epilepsia Open. 2020 Mar 12;5(2):138-154. doi: 10.1002/epi4.12386. eCollection 2020 Jun.
2
Pilocarpine-induced status epilepticus reduces chemosensory control of breathing.毛果芸香碱诱导的癫痫持续状态降低了呼吸的化学感受控制。
Brain Res Bull. 2020 Aug;161:98-105. doi: 10.1016/j.brainresbull.2020.05.002. Epub 2020 May 17.
3
Pilocarpine Induced Behavioral and Biochemical Alterations in Chronic Seizure-Like Condition in Adult Zebrafish.毛果芸香碱诱导成年斑马鱼慢性癫痫样状态下的行为和生化改变。
Int J Mol Sci. 2020 Apr 3;21(7):2492. doi: 10.3390/ijms21072492.
4
Amyloid-β precursor protein mutant zebrafish exhibit seizure susceptibility that depends on prion protein.淀粉样β前体蛋白突变型斑马鱼表现出易发性癫痫,这取决于朊病毒蛋白。
Exp Neurol. 2020 Jun;328:113283. doi: 10.1016/j.expneurol.2020.113283. Epub 2020 Mar 9.
5
Serum α-synuclein and IL-1β are increased and correlated with measures of disease severity in children with epilepsy: potential prognostic biomarkers?血清 α-突触核蛋白和白细胞介素-1β 在癫痫患儿中升高,并与疾病严重程度的测量指标相关:潜在的预后生物标志物?
BMC Neurol. 2020 Mar 9;20(1):85. doi: 10.1186/s12883-020-01662-y.
6
The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration.路易体的形成过程,而不仅仅是α-突触核蛋白的纤维化,是神经退行性变的主要驱动因素之一。
Proc Natl Acad Sci U S A. 2020 Mar 3;117(9):4971-4982. doi: 10.1073/pnas.1913904117. Epub 2020 Feb 19.
7
β-Lapachone attenuates cognitive impairment and neuroinflammation in beta-amyloid induced mouse model of Alzheimer's disease.β-拉帕醌可减轻β-淀粉样蛋白诱导的阿尔茨海默病小鼠模型的认知障碍和神经炎症。
Int Immunopharmacol. 2020 Apr;81:106300. doi: 10.1016/j.intimp.2020.106300. Epub 2020 Feb 15.
8
Transcriptional Regulation of Channelopathies in Genetic and Acquired Epilepsies.遗传性和获得性癫痫中通道病的转录调控
Front Cell Neurosci. 2020 Jan 14;13:587. doi: 10.3389/fncel.2019.00587. eCollection 2019.
9
Epilepsy and brain channelopathies from infancy to adulthood.癫痫和脑通道病:从婴儿期到成年期。
Neurol Sci. 2020 Apr;41(4):749-761. doi: 10.1007/s10072-019-04190-x. Epub 2019 Dec 14.
10
Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy.与颞叶癫痫认知障碍相关的阿尔茨海默样淀粉样蛋白和tau 改变。
Brain. 2020 Jan 1;143(1):191-209. doi: 10.1093/brain/awz381.

重新审视神经退行性变蛋白在癫痫中的作用:聚焦于α-突触核蛋白、β-淀粉样蛋白和tau蛋白。

Revisiting the Impact of Neurodegenerative Proteins in Epilepsy: Focus on Alpha-Synuclein, Beta-Amyloid, and Tau.

作者信息

Paudel Yam Nath, Angelopoulou Efthalia, Piperi Christina, Othman Iekhsan, Shaikh Mohd Farooq

机构信息

Neuropharmacology Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor 47500, Malaysia.

Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street, 11527 Athens, Greece.

出版信息

Biology (Basel). 2020 Jun 12;9(6):122. doi: 10.3390/biology9060122.

DOI:10.3390/biology9060122
PMID:32545604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7344698/
Abstract

Lack of disease-modifying therapy against epileptogenesis reflects the complexity of the disease pathogenesis as well as the high demand to explore novel treatment strategies. In the pursuit of developing new therapeutic strategies against epileptogenesis, neurodegenerative proteins have recently gained increased attention. Owing to the fact that neurodegenerative disease and epileptogenesis possibly share a common underlying mechanism, targeting neurodegenerative proteins against epileptogenesis might represent a promising therapeutic approach. Herein, we review the association of neurodegenerative proteins, such as α-synuclein, amyloid-beta (Aβ), and tau protein, with epilepsy. Providing insight into the α-synuclein, Aβ and tau protein-mediated neurodegeneration mechanisms, and their implication in epileptogenesis will pave the way towards the development of new agents and treatment strategies.

摘要

缺乏针对癫痫发生的疾病修饰疗法反映了疾病发病机制的复杂性以及探索新治疗策略的高需求。在寻求开发针对癫痫发生的新治疗策略的过程中,神经退行性蛋白最近受到了越来越多的关注。由于神经退行性疾病和癫痫发生可能共享一个共同的潜在机制,针对神经退行性蛋白来对抗癫痫发生可能代表一种有前景的治疗方法。在此,我们综述了神经退行性蛋白,如α-突触核蛋白、β-淀粉样蛋白(Aβ)和tau蛋白与癫痫的关联。深入了解α-突触核蛋白、Aβ和tau蛋白介导的神经退行性变机制及其在癫痫发生中的作用,将为新药物和治疗策略的开发铺平道路。