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BioMed Research International
Volume 2017 (2017), Article ID 8030369, 11 pages
Research Article

Profiling microRNA from Brain by Microarray in a Transgenic Mouse Model of Alzheimer’s Disease

1Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China
2Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, Beijing 100050, China
3Key Laboratory of Uighur Medicine of Xinjiang Uygur Autonomous Region, Xinjiang Institute of Materia Medica, Urumqi 830004, China
4Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China
5Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China

Correspondence should be addressed to Rui Liu; and Shui-long Guo; moc.361@oug.gnols

Received 31 May 2017; Accepted 9 August 2017; Published 19 September 2017

Academic Editor: Alessandro Martorana

Copyright © 2017 Lin-lin Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


MicroRNAs (miRNAs) are small noncoding RNAs, which regulate numerous cell functions by targeting mRNA for cleavage or translational repression, and have been found to play an important role in Alzheimer’s disease (AD). Our study aimed to identify differentially expressed miRNAs in AD brain as a reference of potential therapeutic miRNAs or biomarkers for this disease. We used amyloid precursor protein (APP) and presenilin 1 (PS1) double transgenic mice and age-matched wild-type (WT) littermates to determine the expression of miRNAs in the brain. MiRNAs were profiled by microarray, and differentially expressed miRNAs underwent target prediction and enrichment analysis. Microarray analysis revealed 56 differentially expressed miRNAs in AD mouse brain, which involved 39 miRNAs that were significantly upregulated and 19 that were downregulated at different ages. Among those miRNAs, a total of 11 miRNAs, including miR-342-3p, miR-342-5p, miR-376c-3p, and miR-301b-3p, were not only conserved in human but also predicted to have targets and signaling pathways closely related to the pathology of AD. In conclusion, in this study, differentially expressed miRNAs were identified in AD brain and proposed as biomarkers, which may have the potential to indicate AD progression. Despite being preliminary, these results may aid in investigating pathological hallmarks and identify effective therapeutic targets.