• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

缺氧与阿尔茨海默病的关系:最新综述

The relationship between hypoxia and Alzheimer's disease: an updated review.

作者信息

Tao Borui, Gong Wei, Xu Chengyuan, Ma Zhihui, Mei Jinyu, Chen Ming

机构信息

Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China.

The First Clinical Medical College, Anhui Medical University, Hefei, China.

出版信息

Front Aging Neurosci. 2024 Jul 17;16:1402774. doi: 10.3389/fnagi.2024.1402774. eCollection 2024.

DOI:10.3389/fnagi.2024.1402774
PMID:39086755
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11288848/
Abstract

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases, and the most prevalent form of dementia. The main hallmarks for the diagnosis of AD are extracellular amyloid-beta (Aβ) plaque deposition and intracellular accumulation of highly hyperphosphorylated Tau protein as neurofibrillary tangles. The brain consumes more oxygen than any other organs, so it is more easily to be affected by hypoxia. Hypoxia has long been recognized as one of the possible causes of AD and other neurodegenerative diseases, but the exact mechanism has not been clarified. In this review, we will elucidate the connection between hypoxia-inducible factors-1α and AD, including its contribution to AD and its possible protective effects. Additionally, we will discuss the relationship between oxidative stress and AD as evidence show that oxidative stress acts on AD-related pathogenic factors such as mitochondrial dysfunction, Aβ deposition, inflammation, etc. Currently, there is no cure for AD. Given the close association between hypoxia, oxidative stress, and AD, along with current research on the protective effects of antioxidants against AD, we speculate that antioxidants could be a potential therapeutic approach for AD and worth further study.

摘要

阿尔茨海默病(AD)是最常见的神经退行性疾病之一,也是痴呆最普遍的形式。AD诊断的主要标志是细胞外β淀粉样蛋白(Aβ)斑块沉积以及高度磷酸化的 Tau 蛋白在细胞内积聚形成神经原纤维缠结。大脑比其他任何器官消耗的氧气都多,因此更容易受到缺氧的影响。长期以来,缺氧一直被认为是AD和其他神经退行性疾病的可能病因之一,但确切机制尚未阐明。在本综述中,我们将阐明缺氧诱导因子-1α与AD之间的联系,包括其对AD的作用及其可能的保护作用。此外,我们将讨论氧化应激与AD之间的关系,因为有证据表明氧化应激作用于AD相关的致病因素,如线粒体功能障碍、Aβ沉积、炎症等。目前,AD尚无治愈方法。鉴于缺氧、氧化应激与AD之间的密切关联,以及目前关于抗氧化剂对AD保护作用的研究,我们推测抗氧化剂可能是AD的一种潜在治疗方法,值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/ada1dfc8a87b/fnagi-16-1402774-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/4d8cf416ab8a/fnagi-16-1402774-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/2facc2612b7c/fnagi-16-1402774-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/36d45e1239c8/fnagi-16-1402774-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/ada1dfc8a87b/fnagi-16-1402774-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/4d8cf416ab8a/fnagi-16-1402774-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/2facc2612b7c/fnagi-16-1402774-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/36d45e1239c8/fnagi-16-1402774-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa82/11288848/ada1dfc8a87b/fnagi-16-1402774-g004.jpg

相似文献

1
The relationship between hypoxia and Alzheimer's disease: an updated review.缺氧与阿尔茨海默病的关系:最新综述
Front Aging Neurosci. 2024 Jul 17;16:1402774. doi: 10.3389/fnagi.2024.1402774. eCollection 2024.
2
Therapeutic potentials of plant iridoids in Alzheimer's and Parkinson's diseases: A review.植物环烯醚萜类化合物在阿尔茨海默病和帕金森病中的治疗潜力:综述。
Eur J Med Chem. 2019 May 1;169:185-199. doi: 10.1016/j.ejmech.2019.03.009. Epub 2019 Mar 8.
3
Role of Hypoxia Inducible Factor-1α in Alzheimer's Disease.缺氧诱导因子-1α 在阿尔茨海默病中的作用。
J Alzheimers Dis. 2021;80(3):949-961. doi: 10.3233/JAD-201448.
4
A Recent Update on Pathophysiology and Therapeutic Interventions of Alzheimer's Disease.阿尔茨海默病的病理生理学和治疗干预的最新进展。
Curr Pharm Des. 2023;29(43):3428-3441. doi: 10.2174/0113816128264355231121064704.
5
Hypoxia-inducible factors as neuroprotective agent in Alzheimer's disease.缺氧诱导因子作为阿尔茨海默病的神经保护剂
Clin Exp Pharmacol Physiol. 2017 Mar;44(3):327-334. doi: 10.1111/1440-1681.12717.
6
HIF-1α serves as a co-linker between AD and T2DM.HIF-1α 作为 AD 和 T2DM 之间的共同连接物。
Biomed Pharmacother. 2024 Feb;171:116158. doi: 10.1016/j.biopha.2024.116158. Epub 2024 Jan 18.
7
Role of mitochondrial dysfunction, oxidative stress and autophagy in progression of Alzheimer's disease.线粒体功能障碍、氧化应激和自噬在阿尔茨海默病进展中的作用。
J Neurol Sci. 2021 Feb 15;421:117253. doi: 10.1016/j.jns.2020.117253. Epub 2020 Dec 5.
8
Insights from on Aβ- and tau-induced mitochondrial dysfunction: mechanisms and tools.关于Aβ和tau蛋白诱导的线粒体功能障碍的见解:机制与工具
Front Neurosci. 2023 Apr 17;17:1184080. doi: 10.3389/fnins.2023.1184080. eCollection 2023.
9
Alzheimer's disease.阿尔茨海默病
Subcell Biochem. 2012;65:329-52. doi: 10.1007/978-94-007-5416-4_14.
10
Alzheimer's Disease is Driven by Intraneuronally Retained Beta-Amyloid Produced in the AD-Specific, βAPP-Independent Pathway: Current Perspective and Experimental Models for Tomorrow.阿尔茨海默病由在AD特异性、β-淀粉样前体蛋白(βAPP)非依赖途径中产生并在神经元内保留的β-淀粉样蛋白驱动:当前观点及未来实验模型
Ann Integr Mol Med. 2020;2(1):90-114. doi: 10.33597/aimm.02-1007.

引用本文的文献

1
The Potential Regulators of Amyloidogenic Pathway of APP Processing in Alzheimer's Disease.阿尔茨海默病中APP加工淀粉样蛋白生成途径的潜在调节因子
Biomedicines. 2025 Jun 20;13(7):1513. doi: 10.3390/biomedicines13071513.
2
Dysregulation of cerebral perfusion dynamics is associated with Alzheimer's disease.脑灌注动力学失调与阿尔茨海默病相关。
Alzheimers Dement (Amst). 2025 Jul 18;17(3):e70134. doi: 10.1002/dad2.70134. eCollection 2025 Jul-Sep.
3
Low-dose dietary vorinostat increases brain histone acetylation levels and reduces oxidative stress in an Alzheimer's disease mouse model.

本文引用的文献

1
2024 Alzheimer's disease facts and figures.2024 年阿尔茨海默病事实和数据。
Alzheimers Dement. 2024 May;20(5):3708-3821. doi: 10.1002/alz.13809. Epub 2024 Apr 30.
2
HIF-1α is a "brake" in JNK-mediated activation of amyloid protein precursor and hyperphosphorylation of tau induced by T-2 toxin in BV2 cells.缺氧诱导因子 1α(HIF-1α)是 T-2 毒素在 BV2 细胞中引起的淀粉样蛋白前体 JNK 介导的激活和过度磷酸化tau 的“刹车”。
Mycotoxin Res. 2024 May;40(2):223-234. doi: 10.1007/s12550-024-00525-6. Epub 2024 Feb 6.
3
Chronic intermittent hypoxia induces cognitive impairment in Alzheimer's disease mouse model via postsynaptic mechanisms.
低剂量饮食伏立诺他可提高阿尔茨海默病小鼠模型的脑组蛋白乙酰化水平并减轻氧化应激。
J Alzheimers Dis. 2025 Jul 1;106(4):13872877251352107. doi: 10.1177/13872877251352107.
4
Targeting hypoxia-related pathobiology in Alzheimer's disease: strategies for prevention and treatment.针对阿尔茨海默病中与缺氧相关的病理生物学:预防和治疗策略。
Mol Biol Rep. 2025 Apr 23;52(1):416. doi: 10.1007/s11033-025-10520-4.
5
Therapeutic Mechanisms of Medicine Food Homology Plants in Alzheimer's Disease: Insights from Network Pharmacology, Machine Learning, and Molecular Docking.药食同源植物在阿尔茨海默病中的治疗机制:基于网络药理学、机器学习和分子对接的见解
Int J Mol Sci. 2025 Feb 27;26(5):2121. doi: 10.3390/ijms26052121.
慢性间歇性低氧通过突触后机制诱导阿尔茨海默病小鼠模型的认知障碍。
Sleep Breath. 2024 Jun;28(3):1197-1205. doi: 10.1007/s11325-023-02970-6. Epub 2024 Jan 24.
4
Inflammatory Processes in Alzheimer's Disease-Pathomechanism, Diagnosis and Treatment: A Review.阿尔茨海默病中的炎症过程——发病机制、诊断和治疗:综述。
Int J Mol Sci. 2023 Mar 30;24(7):6518. doi: 10.3390/ijms24076518.
5
Relationship of Apolipoprotein E with Alzheimer's Disease and Other Neurological Disorders: An Updated Review.载脂蛋白E与阿尔茨海默病及其他神经疾病的关系:最新综述
Neuroscience. 2023 Mar 15;514:123-140. doi: 10.1016/j.neuroscience.2023.01.032. Epub 2023 Feb 2.
6
HIF-1α Causes LCMT1/PP2A Deficiency and Mediates Tau Hyperphosphorylation and Cognitive Dysfunction during Chronic Hypoxia.低氧诱导因子 1α(HIF-1α)导致 LCMT1/PP2A 缺乏,并介导慢性缺氧时的 Tau 过度磷酸化和认知功能障碍。
Int J Mol Sci. 2022 Dec 17;23(24):16140. doi: 10.3390/ijms232416140.
7
HIF-1α Regulates Bone Homeostasis and Angiogenesis, Participating in the Occurrence of Bone Metabolic Diseases.HIF-1α 调节骨稳态和血管生成,参与骨代谢疾病的发生。
Cells. 2022 Nov 10;11(22):3552. doi: 10.3390/cells11223552.
8
SYK coordinates neuroprotective microglial responses in neurodegenerative disease.SYK 协调神经退行性疾病中的神经保护小胶质细胞反应。
Cell. 2022 Oct 27;185(22):4135-4152.e22. doi: 10.1016/j.cell.2022.09.030. Epub 2022 Oct 17.
9
The Tryptophan Catabolite or Kynurenine Pathway in Alzheimer's Disease: A Systematic Review and Meta-Analysis.阿尔茨海默病色氨酸分解产物或犬尿氨酸途径:系统评价和荟萃分析。
J Alzheimers Dis. 2022;88(4):1325-1339. doi: 10.3233/JAD-220295.
10
Hypoxia Inducible Factor-1α binds and activates γ-secretase for Aβ production under hypoxia and cerebral hypoperfusion.缺氧诱导因子-1α在缺氧和脑低灌注下结合并激活 γ-分泌酶产生 Aβ。
Mol Psychiatry. 2022 Oct;27(10):4264-4273. doi: 10.1038/s41380-022-01676-7. Epub 2022 Jun 28.