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阿尔茨海默病中微小RNA的调控

The Regulation of microRNAs in Alzheimer's Disease.

作者信息

Kou Xianjuan, Chen Dandan, Chen Ning

机构信息

Hubei Key Laboratory of Exercise Training and Monitoring, Tianjiu Research and Development Center for Exercise Nutrition and Foods, College of Health Science, Wuhan Sports University, Wuhan, China.

出版信息

Front Neurol. 2020 Apr 17;11:288. doi: 10.3389/fneur.2020.00288. eCollection 2020.

DOI:10.3389/fneur.2020.00288
PMID:32362867
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7180504/
Abstract

MicroRNAs are small non-coding nucleic acids that are responsible for regulating the gene expression by binding to the coding region and 3' and 5' un-translated region of target messenger RNA. Approximately 70% of known microRNAs are expressed in the brain and increasing evidences demonstrate the possible involvement of microRNAs in Alzheimer's disease (AD) according to the statistics. The characteristic symptoms of AD are the progressive loss of memory and cognitive functions due to the deposition of amyloid β (Aβ) peptide, intracellular aggregation of hyperphosphorylated Tau protein, the loss of synapses, and neuroinflammation, as well as dysfunctional autophagy. Therefore, microRNA-mediated regulation for above-mentioned changes may be the potential therapeutic strategies for AD. In this review, the role of specific microRNAs involved in AD and corresponding applications are systematically discussed, including positive effects associated with the reduction of Aβ or Tau protein, the protection of synapses, the inhibition of neuroinflammation, the mitigation of aging, and the induction of autophagy in AD. It will be beneficial to develop effective targets for establishing a cross link between pharmacological intervention and AD in the near future.

摘要

微小RNA是一类小的非编码核酸,通过与靶信使核糖核酸的编码区以及3'和5'非翻译区结合来调控基因表达。据统计,约70%的已知微小RNA在大脑中表达,越来越多的证据表明微小RNA可能参与阿尔茨海默病(AD)。AD的特征性症状是由于淀粉样β(Aβ)肽沉积、细胞内过度磷酸化 Tau 蛋白聚集、突触丧失、神经炎症以及自噬功能障碍导致的记忆和认知功能进行性丧失。因此,微小RNA介导的对上述变化的调控可能是AD的潜在治疗策略。在本综述中,系统地讨论了参与AD的特定微小RNA的作用及其相应应用,包括与减少Aβ或Tau蛋白、保护突触、抑制神经炎症、减轻衰老以及诱导AD自噬相关的积极作用。这将有利于在不久的将来开发有效的靶点,以建立药物干预与AD之间的联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04ee/7180504/c0a7e2ed8568/fneur-11-00288-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04ee/7180504/c0a7e2ed8568/fneur-11-00288-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/04ee/7180504/c0a7e2ed8568/fneur-11-00288-g0001.jpg

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