| First Author | Luo H | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 8 | Pages | e101725 |
| PubMed ID | 25148207 | Mgi Jnum | J:221085 |
| Mgi Id | MGI:5637900 | Doi | 10.1371/journal.pone.0101725 |
| Citation | Luo H, et al. (2014) Genome-wide analysis of miRNA signature in the APPswe/PS1DeltaE9 mouse model of alzheimer's disease. PLoS One 9(8):e101725 |
| abstractText | Alzheimer's disease (AD) is the most common cause of dementia. One of the pathological hallmarks of AD is amyloid beta (Abeta) deposition. MicroRNAs (miRNAs) are small non-coding RNAs whose expression levels change significantly during neuronal pathogenesis and may be used as diagnostic markers. Some miRNAs are important in AD development by targeting genes responsible for Abeta metabolism. However, a systematic assessment of the miRNA expression profile induced by Abeta-mediated neuronal pathogenesis is still lacking. In the present study, we examined miRNA expression profile by using the APPswe/PS1DeltaE9 mouse model of AD. Two sibling pairs of mice were examined, showing 30 and 24 miRNAs with significantly altered expression levels from each paired control, respectively. Nine known miRNAs were common in both groups. Prediction of putative target genes and functional annotation implied that these altered miRNAs affect many target genes mainly involved in PI3K/Akt signaling pathway. This study provides a general profile of miRNAs regulated by Abeta-associated signal pathways, which is helpful to understand the mechanism of Abeta-induced neuronal dysfunction in AD development. |
