Role and relation of cell death in Alzheimer's disease.

3区 生物学 Q2 Biochemistry, Genetics and Molecular Biology
Duc Anh Hoang, Duc Anh Le, Thi My Hanh Do, Van Thai Than
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引用次数: 0

Abstract

Alzheimer's disease (AD), caused by damage to the brain's nerve cells, is a progressive neurodegenerative disease that insidiously erodes cognitive function, and primarily affecting elderly adults. AD is associated with a considerable economic burden arising from multiple expenditure categories. The programed cell death, in normal cells, plays importance roles in biological processes, ensuring homeostasis and controlling development in multicellular organisms. However, AD is characterized by a high degree of pathological-related neuronal death, which is observable in various regions of the brain. This chapter aims to examine the diverse forms of cell death involved in AD, including apoptosis, necroptosis, autophagy-related cell death, and excitotoxicity; as well as elucidates the molecular mechanisms linking cell death to AD pathogenesis, including amyloid-beta, tau pathology, neuroinflammation, mitochondrial dysfunction, and genetic factors. Targeting these cell death pathways offers a promising avenue for future AD therapeutics and drug development.

细胞死亡在阿尔茨海默病中的作用和关系。
阿尔茨海默病(AD)是一种由大脑神经细胞损伤引起的进行性神经退行性疾病,它会潜移默化地侵蚀认知功能,主要影响老年人。AD与多种支出类别造成的相当大的经济负担有关。在正常细胞中,程序性细胞死亡在生物过程中起着重要的作用,保证了多细胞生物的体内平衡并控制了其发育。然而,阿尔茨海默病的特点是高度的病理性相关神经元死亡,这在大脑的各个区域都可以观察到。本章旨在研究AD中涉及的各种形式的细胞死亡,包括凋亡、坏死坏死、自噬相关的细胞死亡和兴奋毒性;并阐明了将细胞死亡与AD发病机制联系起来的分子机制,包括淀粉样蛋白- β、tau病理、神经炎症、线粒体功能障碍和遗传因素。靶向这些细胞死亡途径为未来的阿尔茨海默病治疗和药物开发提供了一条有希望的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.00
自引率
0.00%
发文量
110
审稿时长
4-8 weeks
期刊介绍: Progress in Molecular Biology and Translational Science (PMBTS) provides in-depth reviews on topics of exceptional scientific importance. If today you read an Article or Letter in Nature or a Research Article or Report in Science reporting findings of exceptional importance, you likely will find comprehensive coverage of that research area in a future PMBTS volume.
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