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氧化应激、线粒体与胰岛素在阿尔茨海默病中作用的综合观点

An integrative view of the role of oxidative stress, mitochondria and insulin in Alzheimer's disease.

作者信息

Moreira Paula I, Duarte Ana I, Santos Maria S, Rego A Cristina, Oliveira Catarina R

机构信息

Center for Neuroscience and Cell Biology, Faculty of Medicine, Institute of Physiology, Department of Zoology, University of Coimbra, Coimbra, Portugal.

出版信息

J Alzheimers Dis. 2009;16(4):741-61. doi: 10.3233/JAD-2009-0972.

Abstract

The processes underlying the pathogenesis of Alzheimer's disease involve several factors including impaired glucose/energy metabolism, mitochondrial dysfunction, oxidative stress and altered insulin-signaling pathways. This review is mainly devoted to discuss evidence supporting the notion that mitochondrial dysfunction and oxidative stress are interconnected and intimately associated with the development and progression of Alzheimer's disease. Furthermore, the review explores the role of insulin signaling in the pathophysiology of the disease. Indeed, several studies have begun to find links between insulin and mechanisms with clear pathogenic implications for this disorder. Understanding the key mechanisms involved in the etiopathogenesis of Alzheimer's disease may provide opportunities for the design of efficacious preventive and therapeutic strategies.

摘要

阿尔茨海默病发病机制背后的过程涉及多个因素,包括葡萄糖/能量代谢受损、线粒体功能障碍、氧化应激和胰岛素信号通路改变。本综述主要致力于讨论支持线粒体功能障碍和氧化应激相互关联且与阿尔茨海默病的发生和发展密切相关这一观点的证据。此外,该综述还探讨了胰岛素信号在该疾病病理生理学中的作用。事实上,一些研究已开始发现胰岛素与对该病症具有明确致病意义的机制之间的联系。了解阿尔茨海默病病因发病机制中涉及的关键机制可能为设计有效的预防和治疗策略提供机会。

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