Brief intro:
- Author: Xin Feng, Bo-Wen Jiang, Si-Nan Zhai, Chu-Xiao Liu, Hao Wu, Bang-Qi Zhu, Meng-Yuan Wei, Jia Wei, Li Yang, Ling-Ling Chen
- Journal: BioRxiv
- Doi: https://www.doi.org/10.1101/2024.03.27.583257
- Publication Date: 2024 Mar 24
Products/Services used in the paper
Quotation shows PackGene:The overexpressed virus AAV2/9 and AAV-MG1.2 used in this study was packaged 27 and produced by BrainVT A (Wuhan) Co., Ltd, AAV-PHP.eB was packaged and 28 (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. The copyright holder for this preprint this version posted March 27, 2024. ; https://doi.org/10.1101/2024.03.27.583257 doi: bioRxiv preprint 14 produced by Guangzhou PackGene Biotech Co., Ltd and BrainVT A (Wuhan) Co., 1 LTD
Research Field:Alzheimer's
AAV Serotype:AAV-PHP.eB
Targeted organ:brain
Animal or cell line strain:mice
Abstract
Here, we delineated the remarkably elevated neuroinflammation accompanied by progressive activation of double-stranded RNA (dsRNA)-activated Protein Kinase R (PKR) and PKR-related dsRNA pathways in hippocampus of 5×FAD mice upon Alzheimer’s disease (AD) progression. AAV-delivery of circular RNAs possessing short-imperfect duplex regions (ds-cRNAs) to neurons and microglia effectively dampened excessive PKR activity with little toxicity, accompanying with reduced neuroinflammation and amyloid-beta (Aβ) plaques, resulting in neuroprotection and enhanced capability of spatial learning and memory in AD mouse models. These findings suggest a therapeutic potential of ds-cRNA aptamers as PKR inhibitors in AD therapy.
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