Research Paper Volume 10, Issue 2 pp 253—265
Comprehensive analysis of differentially expressed profiles of Alzheimer’s disease associated circular RNAs in an Alzheimer’s disease mouse model
- 1 Department of Pharmacology, Pharmacy School, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China
- 2 Scientific research center of traditional Chinese medicine, Guangxi University of Chinese Medicine, Nanning, Guangxi 530200, China
- 3 Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Pharmacy School, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China
- 4 Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530200, China
Received: December 28, 2017 Accepted: February 9, 2018 Published: February 15, 2018
https://doi.org/10.18632/aging.101387How to Cite
Abstract
Circular RNAs (circRNAs), a novel kind of non-coding RNA, have received increasing attention for their involvement in pathogenesis of Alzheimer’s disease (AD); however, few studies have reported in the characterization and function of AD associated circRNAs. Here the expression profiles of circRNAs in 5- and 10-month-old SAMP8 mice were identified using circRNA microarray and found that 85 dysregulated circRNAs were observed in 10-month-old SAMP8 versus control mice and 231 circRNAs exhibited differential expression in 10-month-old SAMP8 versus 5-month-old SAMP8. One most significantly dysregulated circRNA, mmu_circRNA_017963, was select for Gene Oncology (GO) and pathway analysis. The results showed that mmu_circRNA_017963 was strongly related with autophagosome assembly, exocytosis, apoptotic process, transport and RNA splicing and highly associated with synaptic vesicle cycle, spliceosome, glycosaminoglycan and SNARE interactions in vesicular transport pathways. Collectively, this study was the first to describe circRNAs expression in different ages of SAMP8 and will contribute to the understanding of the regulatory roles of circRNAs in AD pathogenesis and provide a valuable resource for the diagnosis and therapy of AD.