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辅酶Q与阿尔茨海默病中的线粒体功能障碍

CoQ and Mitochondrial Dysfunction in Alzheimer's Disease.

作者信息

Fišar Zdeněk, Hroudová Jana

机构信息

Department of Psychiatry, First Faculty of Medicine, Charles University and General University Hospital in Prague, Ke Karlovu 11, 120 00 Prague, Czech Republic.

出版信息

Antioxidants (Basel). 2024 Feb 2;13(2):191. doi: 10.3390/antiox13020191.

DOI:10.3390/antiox13020191
PMID:38397789
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10885987/
Abstract

The progress in understanding the pathogenesis and treatment of Alzheimer's disease (AD) is based on the recognition of the primary causes of the disease, which can be deduced from the knowledge of risk factors and biomarkers measurable in the early stages of the disease. Insights into the risk factors and the time course of biomarker abnormalities point to a role for the connection of amyloid beta (Aβ) pathology, tau pathology, mitochondrial dysfunction, and oxidative stress in the onset and development of AD. Coenzyme Q (CoQ) is a lipid antioxidant and electron transporter in the mitochondrial electron transport system. The availability and activity of CoQ is crucial for proper mitochondrial function and cellular bioenergetics. Based on the mitochondrial hypothesis of AD and the hypothesis of oxidative stress, the regulation of the efficiency of the oxidative phosphorylation system by means of CoQ can be considered promising in restoring the mitochondrial function impaired in AD, or in preventing the onset of mitochondrial dysfunction and the development of amyloid and tau pathology in AD. This review summarizes the knowledge on the pathophysiology of AD, in which CoQ may play a significant role, with the aim of evaluating the perspective of the pharmacotherapy of AD with CoQ and its analogues.

摘要

对阿尔茨海默病(AD)发病机制和治疗的认识进展基于对该疾病主要病因的认识,这些病因可从疾病早期可测量的风险因素和生物标志物的知识中推导出来。对风险因素和生物标志物异常时间进程的深入了解表明,淀粉样β蛋白(Aβ)病理、tau病理、线粒体功能障碍和氧化应激之间的联系在AD的发病和发展中起作用。辅酶Q(CoQ)是线粒体电子传递系统中的一种脂质抗氧化剂和电子转运体。CoQ的可用性和活性对于正常的线粒体功能和细胞生物能量学至关重要。基于AD的线粒体假说和氧化应激假说,通过CoQ调节氧化磷酸化系统的效率有望恢复AD中受损的线粒体功能,或预防AD中线粒体功能障碍的发生以及淀粉样和tau病理的发展。本综述总结了CoQ可能发挥重要作用的AD病理生理学知识,旨在评估用CoQ及其类似物进行AD药物治疗的前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/1ee65cebceaf/antioxidants-13-00191-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/aa80e130347d/antioxidants-13-00191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/007fa41e27b1/antioxidants-13-00191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/24d18500e7c4/antioxidants-13-00191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/1ee65cebceaf/antioxidants-13-00191-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/aa80e130347d/antioxidants-13-00191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/007fa41e27b1/antioxidants-13-00191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/24d18500e7c4/antioxidants-13-00191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0636/10885987/1ee65cebceaf/antioxidants-13-00191-g004.jpg

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