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阿尔茨海默病中氧化应激的分子机制与遗传学

Molecular Mechanisms and Genetics of Oxidative Stress in Alzheimer's Disease.

作者信息

Cioffi Federica, Adam Rayan Hassan Ibrahim, Broersen Kerensa

机构信息

Nanobiophysics Group, Technical Medical Centre, Faculty of Science and Technology, University of Twente, Enschede, The Netherlands.

Applied Stem Cell Technologies, Technical Medical Centre, Faculty of Science and Technology, University of Twente, Enschede, The Netherlands.

出版信息

J Alzheimers Dis. 2019;72(4):981-1017. doi: 10.3233/JAD-190863.

DOI:10.3233/JAD-190863
PMID:31744008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6971833/
Abstract

Alzheimer's disease is the most common neurodegenerative disorder that can cause dementia in elderly over 60 years of age. One of the disease hallmarks is oxidative stress which interconnects with other processes such as amyloid-β deposition, tau hyperphosphorylation, and tangle formation. This review discusses current thoughts on molecular mechanisms that may relate oxidative stress to Alzheimer's disease and identifies genetic factors observed from in vitro, in vivo, and clinical studies that may be associated with Alzheimer's disease-related oxidative stress.

摘要

阿尔茨海默病是最常见的神经退行性疾病,可导致60岁以上老年人痴呆。该疾病的标志之一是氧化应激,它与其他过程相互关联,如淀粉样β蛋白沉积、tau蛋白过度磷酸化和缠结形成。本文综述了关于氧化应激与阿尔茨海默病可能相关的分子机制的当前观点,并确定了在体外、体内和临床研究中观察到的可能与阿尔茨海默病相关氧化应激有关的遗传因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42a2/6971833/bf803f3e4868/jad-72-jad190863-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42a2/6971833/bf803f3e4868/jad-72-jad190863-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42a2/6971833/bf803f3e4868/jad-72-jad190863-g001.jpg

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