摘要
在神经退行性疾病中,身体有进行性退行性变,导致神经细胞死亡。在这种状态下,患者每天都会患有精神虚弱、痴呆和共济失调。阿尔茨海默病(AD)是最常见的不可逆神经退行性脑疾病,主要影响65岁以上的人。许多类型的研究表明,AD的主要罪魁祸首是一种被称为淀粉样蛋白的(39-43)氨基酸肽的聚集形式。淀粉样蛋白(Aβ)是由分泌酶和分泌酶对较大的糖蛋白的作用产生的。Gamma(γ)分泌酶是一种膜内蛋白酶复合物,它可以切割单通道跨膜蛋白、淀粉样前体蛋白和Notch。γ-分泌酶复合物包含早老素、早老素增强因子2、前咽缺陷因子1和尼卡斯汀。任何早老素-1的突变或γ分泌酶直接或间接切割淀粉样前体蛋白都与AD相关。因此,预防这种酶是治疗AD的溶液之一。在这篇文章中,我们讨论了γ-分泌酶复合物及其抑制剂,可以有助于预防AD。
关键词: 神经退行性疾病、阿尔茨海默病、淀粉样蛋白、γ分泌酶、Notch、早衰老素、前咽缺陷-1、尼卡斯特蛋白、淀粉样前体蛋白。
图形摘要
Current Drug Targets
Title:Insight γ-Secretase: Structure, Function, and Role in Alzheimer’s Disease
Volume: 22 Issue: 12
关键词: 神经退行性疾病、阿尔茨海默病、淀粉样蛋白、γ分泌酶、Notch、早衰老素、前咽缺陷-1、尼卡斯特蛋白、淀粉样前体蛋白。
摘要: In neurodegenerative disorders, there is a progressive degeneration of the body, leading to the death of nerve cells. In this state, a patient gets affected day by day with mental weakness, dementia, and ataxia. Alzheimer’s disease (AD) is the most common irreversible neurodegenerative brain disorder mainly affecting people over the age of 65. Many types of research suggest that the main culprit for AD is the aggregated form of a (39-43) amino acid peptide called amyloid beta. Amyloid beta (Aβ) is generated by the action of beta-secretase and gamma-secretase on the larger glycoprotein. Gamma (γ) secretase is an intra-membrane protease complex that cleaves the single-- pass transmembrane protein, the amyloid precursor protein, and Notch. The γ-secretase complex contains presenilin, presenilin enhancer-2, anterior pharynx defective-1, and nicastrin. Any mutation in presenilin-1 or the cleavage of amyloid precursor protein by γ-secretase directly or indirectly is associated with AD. Therefore, the prevention of this enzyme is one of the solutions for AD. In this article, we discuss the γ-secretase complex and its inhibitors that can contribute to the prevention of AD.
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Cite this article as:
Insight γ-Secretase: Structure, Function, and Role in Alzheimer’s Disease, Current Drug Targets 2021; 22 (12) . https://dx.doi.org/10.2174/1389450121999201230203709
DOI https://dx.doi.org/10.2174/1389450121999201230203709 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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