Journal
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2021.719247
Keywords
long non-coding RNAs; neurodegenerative diseases; Alzheimer's disease; Parkinson's disease; Huntington's disease; amyotrophic lateral sclerosis
Categories
Funding
- Shandong Provincial Natural Science Foundation China [ZR2015HM024, 2019GSF108066]
- SFR
- IIFDU [11681701]
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Emerging evidence suggests that aberrant epigenetic regulation of gene expression is linked to the pathogenesis of neurological disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. Long non-coding RNAs (lncRNAs), with lengths of 200 nt or more, play crucial roles in regulating various biological processes and contribute to the development of diseases at transcriptional and post-transcriptional levels. This review focuses on the latest research progress regarding how lncRNAs contribute to the pathogenesis of neurodegenerative diseases through mechanisms like autophagy regulation, A beta deposition, neuroinflammation, Tau phosphorylation, and alpha-synuclein aggregation, while also highlighting the challenges in studying lncRNA-mediated epigenetics to understand the molecular mechanisms of these diseases further.
Emerging evidence addresses the link between the aberrant epigenetic regulation of gene expression and numerous diseases including neurological disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD). LncRNAs, a class of ncRNAs, have length of 200 nt or more, some of which crucially regulate a variety of biological processes such as epigenetic-mediated chromatin remodeling, mRNA stability, X-chromosome inactivation and imprinting. Aberrant regulation of the lncRNAs contributes to pathogenesis of many diseases, such as the neurological disorders at the transcriptional and post-transcriptional levels. In this review, we highlight the latest research progress on the contributions of some lncRNAs to the pathogenesis of neurodegenerative diseases via varied mechanisms, such as autophagy regulation, A beta deposition, neuroinflammation, Tau phosphorylation and alpha-synuclein aggregation. Meanwhile, we also address the potential challenges on the lncRNAs-mediated epigenetic study to further understand the molecular mechanism of the neurodegenerative diseases.
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