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靶向聚集物自噬治疗阿尔茨海默病。

Targeting Aggrephagy for the Treatment of Alzheimer's Disease.

机构信息

Mr. and Mrs. Ko Chi Ming Centre for Parkinson's Disease Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.

Medical College of Acupuncture-Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.

出版信息

Cells. 2020 Jan 28;9(2):311. doi: 10.3390/cells9020311.

DOI:10.3390/cells9020311
PMID:32012902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7072705/
Abstract

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases in older individuals with specific neuropsychiatric symptoms. It is a proteinopathy, pathologically characterized by the presence of misfolded protein (Aβ and Tau) aggregates in the brain, causing progressive dementia. Increasing studies have provided evidence that the defect in protein-degrading systems, especially the autophagy-lysosome pathway (ALP), plays an important role in the pathogenesis of AD. Recent studies have demonstrated that AD-associated protein aggregates can be selectively recognized by some receptors and then be degraded by ALP, a process termed aggrephagy. In this study, we reviewed the role of aggrephagy in AD development and discussed the strategy of promoting aggrephagy using small molecules for the treatment of AD.

摘要

阿尔茨海默病(AD)是老年人中最常见的神经退行性疾病之一,具有特定的神经精神症状。它是一种蛋白质病,病理特征是大脑中存在错误折叠的蛋白质(Aβ 和 Tau)聚集体,导致进行性痴呆。越来越多的研究提供了证据表明,蛋白质降解系统的缺陷,特别是自噬-溶酶体途径(ALP),在 AD 的发病机制中起着重要作用。最近的研究表明,AD 相关的蛋白聚集体可以被一些受体特异性识别,然后被 ALP 降解,这个过程被称为聚集体自噬。在本研究中,我们综述了聚集体自噬在 AD 发病机制中的作用,并讨论了使用小分子促进聚集体自噬治疗 AD 的策略。

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Animal models of Alzheimer's disease embrace diversity.阿尔茨海默病的动物模型具有多样性。
Lab Anim (NY). 2019 Sep;48(9):255-259. doi: 10.1038/s41684-019-0377-8.
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Modeling Alzheimer's disease with iPSC-derived brain cells.利用 iPSC 衍生脑细胞进行阿尔茨海默病建模。
自噬与阿尔茨海默病:机制及脑外影响
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Comprehensive analysis of autophagy status and its relationship with immunity and inflammation in ischemic stroke through integrated transcriptomic and single-cell sequencing.通过综合转录组学和单细胞测序对缺血性卒中自噬状态及其与免疫和炎症的关系进行综合分析。
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