Abstract
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, Aβ deposition, neuroinflammation, Tau phosphorylation and α-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.
Highlights
Epigenetics literally refers to regulation of gene expression due to external modifications to DNA and histones without altering DNA sequence
Knockdown of SNHG14 expression in MN9D cells could alleviate the damage induced by rotenone in dopaminergic neurons through activation of the miR-133b inhibited by SNHG14, whereas miR-133b targets to 3 UTR of α-synuclein that contributes to Parkinson’s disease (PD) pathogenesis
Accumulated evidence has enabled us to acknowledge that long ncRNAs (lncRNAs) could suppress or promote the neurodegenerative disorders via epigenetically regulating expression of genes crucially involved in the pathogenesis at both transcriptional and posttranscriptional levels
Summary
Epigenetics literally refers to regulation of gene expression due to external modifications to DNA and histones without altering DNA sequence. Lnc-EBF3-AS was maladjusted in late-onset AD patients (Magistri et al, 2015), its upregulation was detected to stimulate the expression of EBF3 in the hippocampus of the AD transgenic mouse model, promoting the apoptosis of neurons in AD (Gu et al, 2018). Another important lncRNA that could be potentially involved in Dopaminergic neuron loss is SNHG14, its expression is upregulated in brain tissue of PD mouse model induced by rotenone.
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