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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.

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。

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