AI Article Synopsis
- Alzheimer's disease (AD) is primarily characterized by the buildup of amyloid β (Aβ) in the brain, which is linked to dementia.
- MicroRNAs (miRNAs) play a critical role in regulating genes that affect Aβ metabolism, and their expression levels change during AD progression, making them potential diagnostic markers.
- The study used a mouse model to identify altered miRNA levels, discovering nine common miRNAs between sibling pairs, which appear to influence genes in the PI3K/Akt signaling pathway, shedding light on Aβ-induced neuronal dysfunction in AD.
Article Abstract
Alzheimer's disease (AD) is the most common cause of dementia. One of the pathological hallmarks of AD is amyloid β (Aβ) 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 Aβ metabolism. However, a systematic assessment of the miRNA expression profile induced by Aβ-mediated neuronal pathogenesis is still lacking. In the present study, we examined miRNA expression profile by using the APPswe/PS1ΔE9 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 Aβ-associated signal pathways, which is helpful to understand the mechanism of Aβ-induced neuronal dysfunction in AD development.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141691 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0101725 | PLOS |
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