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唐氏综合征患者大脑中铜的积累会促进氧化应激：认知障碍潜在的机制。

The accumulation of copper in the brain of Down syndrome promotes oxidative stress: possible mechanism underlying cognitive impairment.

作者信息

Ishihara Keiichi

机构信息

Department of Pathological Biochemistry, Kyoto Pharmaceutical University, 5 Misasagi Nakauchi-cho, Yamashina-ku, Kyoto 607-8414, Japan.

出版信息

J Clin Biochem Nutr. 2022 Jul;71(1):16-21. doi: 10.3164/jcbn.21-155. Epub 2022 Feb 15.

DOI:10.3164/jcbn.21-155
PMID:35903608
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9309086/
Abstract

Individuals with Down syndrome (DS), which is caused by triplication of human chromosome 21 (Hsa21), show numerous characteristic symptoms, such as intellectual disability, an impaired cognitive function, and accelerated aging-like phenotypes. Enhanced oxidative stress is assumed to be implicated as a mechanism underlying many of these symptoms of DS. Some genes coded in Hsa21, such as , , and , are suggested as being involved in the exacerbation of oxidative stress. In addition, enhanced oxidative stress has been recently shown to be caused by dyshomeostasis of the redox-active bio-metal copper in the brain of a mouse model of DS. This review aims to summarize the current knowledge on enhanced oxidative stress in DS and suggest a possible molecular mechanism underlying the cognitive impairment of DS mediated by enhanced oxidative stress.

摘要

唐氏综合征（DS）由人类21号染色体（Hsa21）三体性引起，患者表现出许多特征性症状，如智力残疾、认知功能受损和加速衰老样表型。氧化应激增强被认为是DS许多这些症状的潜在机制。Hsa21编码的一些基因，如 、 和 ，被认为与氧化应激的加剧有关。此外，最近研究表明，氧化应激增强是由DS小鼠模型大脑中具有氧化还原活性的生物金属铜的动态失衡引起的。本综述旨在总结目前关于DS中氧化应激增强的知识，并提出氧化应激增强介导DS认知障碍的可能分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8761/9309086/2f24027d2aac/jcbn21-155f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8761/9309086/46d442ccd33f/jcbn21-155f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8761/9309086/2f24027d2aac/jcbn21-155f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8761/9309086/46d442ccd33f/jcbn21-155f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8761/9309086/2f24027d2aac/jcbn21-155f02.jpg

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本文引用的文献

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Targeting redox-altered plasticity to reactivate synaptic function: A novel therapeutic strategy for cognitive disorder.靶向氧化还原改变的可塑性以重新激活突触功能：一种治疗认知障碍的新策略。
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MicroRNA‑802 increases hepatic oxidative stress and induces insulin resistance in high‑fat fed mice.miR-802 增加高脂喂养小鼠肝脏氧化应激并诱导胰岛素抵抗。
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经鼻给予雷帕霉素恢复异常的 mTOR 信号可减少氧化损伤：在唐氏综合征小鼠模型中关注 HNE 修饰蛋白。
Redox Biol. 2019 May;23:101162. doi: 10.1016/j.redox.2019.101162. Epub 2019 Mar 9.
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Copper accumulation in the brain causes the elevation of oxidative stress and less anxious behavior in Ts1Cje mice, a model of Down syndrome.铜在大脑中的积累导致唐氏综合征模型 Ts1Cje 小鼠氧化应激升高和焦虑行为减少。
Free Radic Biol Med. 2019 Apr;134:248-259. doi: 10.1016/j.freeradbiomed.2019.01.015. Epub 2019 Jan 18.
6
Normalizing the gene dosage of Dyrk1A in a mouse model of Down syndrome rescues several Alzheimer's disease phenotypes.唐氏综合征小鼠模型中 Dyrk1A 基因剂量的正常化可挽救几种阿尔茨海默病表型。
Neurobiol Dis. 2017 Oct;106:76-88. doi: 10.1016/j.nbd.2017.06.010. Epub 2017 Jun 21.
7
Systematic review and meta-analysis shows a specific micronutrient profile in people with Down Syndrome: Lower blood calcium, selenium and zinc, higher red blood cell copper and zinc, and higher salivary calcium and sodium.系统评价和荟萃分析显示唐氏综合征患者存在特定的微量营养素谱：血钙、硒和锌降低，红细胞铜和锌升高，唾液钙和钠升高。
PLoS One. 2017 Apr 19;12(4):e0175437. doi: 10.1371/journal.pone.0175437. eCollection 2017.
8
Increased non-protein bound iron in Down syndrome: contribution to lipid peroxidation and cognitive decline.唐氏综合征中未结合蛋白的铁增加：对脂质过氧化和认知衰退的影响
Free Radic Res. 2016 Dec;50(12):1422-1431. doi: 10.1080/10715762.2016.1253833. Epub 2016 Nov 23.
9
Vitamin E in aging persons with Down syndrome: A randomized, placebo-controlled clinical trial.唐氏综合征老年人补充维生素E：一项随机、安慰剂对照临床试验。
Neurology. 2016 May 31;86(22):2071-6. doi: 10.1212/WNL.0000000000002714. Epub 2016 May 4.
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Modulation of tau phosphorylation by environmental copper.环境铜对 tau 磷酸化的调节。
Transl Neurodegener. 2014 Nov 17;3(1):24. doi: 10.1186/2047-9158-3-24. eCollection 2014.