Insights into the mechanisms of non-coding RNAs’ implication in the pathogenesis of Alzheimer’s disease
DOI:
https://doi.org/10.17179/excli2022-5006Keywords:
Alzheimer’s disease, Hypoxia, ERK, mitochondrial fission, BACE1, miRNAs, lncRNAs, markerAbstract
Non-coding RNAs including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are implicated in the regulation of gene expression at transcriptional, posttranscriptional, and epigenetic levels. Several studies in cell lines, animal models, and humans, have revealed that non-coding RNAs play crucial roles in the pathogenesis of Alzheimer's disease (AD). Detailed knowledge on their mechanism of implication in the AD pathogenesis can help to develop novel therapeutic and disease management strategies. The two main pathological hallmarks of AD are amyloid plaques resulting from the β-amyloid accumulation, and neurofibrillary tangles (NFT) due to the phosphorylated tau accumulation. Several lncRNAs and miRNAs play crucial roles in both these hallmarks of the AD pathogenesis and other AD-related pathological procedures such as neuronal and synaptic plasticity, neuroinflammation, neuronal differentiation and neuronal apoptosis. In this review, we outlined the non-coding RNAs and further discussed how they are implicated in these AD-related pathological procedures.
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Copyright (c) 2022 Majid Khodayi-Shahrak, Mohammad Khalaj-Kondori, Mohammad Ali Hosseinpour Feizi, Mahnaz Talebi
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