Distinct Hippocampal Expression Profiles of Long Non-coding RNAs in an Alzheimer's Disease Model

被引：8

作者：

Yang, Bo ^{[1
]}

Xia, Zi-an ^{[1
,2
]}

Zhong, Bingwu ^{[2
]}

Xiong, Xingui ^{[1
]}

Sheng, Chenxia ^{[2
]}

Wang, Yang ^{[1
]}

Gong, Wei ^{[2
]}

Cao, Yucheng ^{[2
]}

Wang, Zhe ^{[2
]}

Peng, Weijun ^{[2
]}

机构：

[1] Cent South Univ, Xiangya Hosp, Dept Integrated Tradit Chinese & Western Med, Changsha 410008, Hunan, Peoples R China

[2] Cent South Univ, Xiangya Hosp 2, Dept Integrated Tradit Chinese & Western Med, Changsha 410011, Hunan, Peoples R China

来源：

MOLECULAR NEUROBIOLOGY | 2017年 / 54卷 / 07期

基金：

中国国家自然科学基金;

关键词：

Alzheimer's disease; Long non-codingRNAs (lncRNAs); Microarray; Hippocampus; Expression profiles; BRAIN-INJURY; BETA; IDENTIFICATION; MICROARRAY; GENES; LNCRNAS;

D O I：

10.1007/s12035-016-0038-5

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alzheimer's disease (AD), the most prevalent form of dementia worldwide, is a complex neurodegenerative disease characterized by the progressive loss of memory and other cognitive functions. The pathogenesis of AD is not yet completely understood. Although long non-coding RNAs (lncRNAs) have recently been shown to play a role in AD pathogenesis, the specific influences of lncRNAs in AD remain largely unknown; in particular, hippocampal lncRNA expression profiles in AD rats are lacking. In this study, microarray analysis was performed to investigate the hippocampal expression patterns of dysregulated lncRNAs in a rat model of AD. A total of 315 lncRNAs and 311 mRNAs were found to be significantly dysregulated in the AD model (>= 2.0 fold, p < 0.05). Then, quantitative real-time PCR was used to validate the expression of selected lncRNAs and mRNAs. Bioinformatics tools and databases were employed to explore the potential lncRNA functions. This is the first study to comprehensively identify dysregulated hippocampal lncRNAs in AD and to demonstrate the involvement of different lncRNA expression patterns in the hippocampal pathogenesis of AD. This information will enable further research on the pathogenesis of AD and facilitate the development of novel AD therapeutics targeting lncRNAs.

引用

页码：4833 / 4846

页数：14