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Modulating Aβ Fibrillogenesis with ‘Trojan’ peptides
Neuropeptides ( IF 2.5 ) Pub Date : 2020-06-01 , DOI: 10.1016/j.npep.2020.102030
Gaurav Pandey 1 , Sudhir Morla 1 , Sachin Kumar 1 , Vibin Ramakrishnan 1
Affiliation  

Abnormal aggregation of beta-amyloid (Aβ) peptide into amyloid plaques in the brain has been identified as one of the key factors in instigating AD pathogenesis. Inhibition of Aβ aggregation can be an important therapeutic strategy in disease management. In this work, we demonstrate the application of structure-based design of short peptides ('trojan peptides'), intended to intervene in the aggregation of the core recognition domain of amyloid-beta peptide, a known malefactor in Alzheimer's disease. The modulatory effect of trojan peptides has been assessed using ThT fluorescence assay, FETEM imaging, IR, and toxicity assays on model neuronal cell lines. Experimental results suggest that designed trojan peptides could impede the aggregation of the core amyloid fibril forming segment of Aβ peptide, arrest the formation of toxic fibrillar assemblies, and reduce cytotoxicity of the neuronal cell lines.

中文翻译:

用“特洛伊”肽调节 Aβ 原纤维生成

β-淀粉样蛋白 (Aβ) 肽在大脑中异常聚集成淀粉样蛋白斑块已被确定为引发 AD 发病机制的关键因素之一。抑制 Aβ 聚集可能是疾病管理中的重要治疗策略。在这项工作中,我们展示了基于结构的短肽(“特洛伊肽”)设计的应用,旨在干预淀粉样蛋白 β 肽的核心识别域的聚集,淀粉样蛋白 β 肽是阿尔茨海默病中的已知有害因素。木马肽的调节作用已使用 ThT 荧光测定、FETEM 成像、IR 和对模型神经元细胞系的毒性测定进行评估。实验结果表明,设计的木马肽可以阻止 Aβ 肽核心淀粉样原纤维形成片段的聚集,
更新日期:2020-06-01
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