长链非编码RNA在阿尔茨海默病中的研究进展

doi:10.16288/j.yczz.21-427

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Hereditas(Beijing) ›› 2022, Vol. 44 ›› Issue (3): 189-197.doi: 10.16288/j.yczz.21-427

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Research progress on lncRNAs in Alzheimer’s disease

Wandi Xiong¹(), Kaiyu Xu⁴, Lin Lu^1,³, Jiali Li^2,⁴()

1. Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100091, China
2. National Institute on Drug Dependence, Peking University, Beijing 100191, China
3. Peking University Sixth Hospital, Peking University, Beijing 100191, China
4. Key Laboratory of Animal Models and Human Disease Mechanism of Chinese Academy of Science & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China;

Received:2021-12-20 Revised:2022-01-21 Online:2022-03-20 Published:2022-02-16
Contact: Li Jiali E-mail:wandibear@pku.edu.cn;lijiali@mail.kiz.ac.cn
Supported by:
Supported by the National Natural Science Foundation of China(81761128036)

Abstract

Abstract:

Alzheimer’s disease (AD) is the common neurodegenerative disease in the center never system and the typical dementia in old people. The major pathological changes of AD are the accumulation of amyloid-β (Aβ) plaques, neurofibrillary tangles, loss of cholinergic neurons, inflammation and metabolism dysfunction. However, the molecular mechanism leading to AD pathogenesis is not clear. More and more studies reported that long non-coding RNAs (lncRNAs) play important roles in AD. In this review, we briefly introduce the recent research progress on lncRNAs in AD, including their regulation of clearance of the Aβ plaques, synaptic function, inflammation reaction and mitochondrial function, and thus providing the references for that lncRNAs can serve as a potential diagnostic biomarker and therapeutic target in AD.

Key words: lncRNA, Alzheimer’s disease, amyloid-β, synaptic function

Wandi Xiong, Kaiyu Xu, Lin Lu, Jiali Li. Research progress on lncRNAs in Alzheimer’s disease[J]. Hereditas(Beijing), 2022, 44(3): 189-197.

Figures/Tables 4

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Table 1

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名称	表达	作用机制	实验模型	参考文献
BACE1-AS	↑	提高BACE1 mRNA稳定性,增加Aβ₄₂聚积	细胞系,Tg19959小鼠	[20]
51A	↑	下调SORL1,增加Aβ₄₂的聚积	细胞系	[34]
BC200	↑	调控突触后膜局部蛋白质,影响突触功能	AD患者人脑	[24]
BDNF-AS	↑	减少BDNF的表达,神经营养物质耗竭	细胞系,小鼠脑区注射 Aβ₄₂	[35]
NDM29	↑	促进BACE分泌酶的剪切活性,增加Aβ₄₂聚积	细胞系	[31]
17A	↑	影响GABA B信号通路,增加Aβ₄₂的聚积	细胞系	[33]
NEAT1	↑	结合NEDD4L促进PINK1降解,影响线粒体自噬	细胞系,APP/PS1小鼠	[36]
EBF3-AS	↑	促进EBF3上调,促进神经元凋亡	细胞系,APP/PS1小鼠	[37]
SOX21-AS1	↑	上调FZD3/5激活Wnt信号通路,调控突触功能	小鼠脑区注射 Aβ₄₂,原代培养神经元	[38]
ATB	↓	负性调节miR-200,增加Aβ聚积	细胞系	[39]

Research progress on lncRNAs in Alzheimer’s disease

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