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Abstract
Long non-coding RNA (lncRNA) is a kind of non-coding RNA (ncRNA), with a length of 200 nt to 100 kb, that lacks a significant open reading frame (ORF) encoding a protein. lncRNAs are widely implicated in various physiological and pathological processes, such as epigenetic regulation, cell cycle regulation, cell differentiation regulation, cancer, and neurodegenerative diseases, through their interactions with chromatin, protein, and other RNAs. Numerous studies have suggested that lncRNAs are closely linked with the occurrence and development of a variety of diseases, especially neurodegenerative diseases, of which the etiologies are complicated and the underlying mechanisms remain elusive. Determining the roles of lncRNA in the pathogenesis of neurodegenerative diseases will not only deepen understanding of the physiological and pathological processes that occur in those diseases but also provide new ideas and solutions for their diagnosis and prevention. This review aims to highlight the progress of lncRNA research in the pathological and behavioral changes of neurodegenerative diseases. Specifically, we focus on how lncRNA dysfunctions are involved in the pathogenesis of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis.
Highlights
In the human genome, less than 2% of the transcripts encode proteins, and the remaining 98%–99% are non-coding RNAs .1 ncRNAs can be divided into two categories: short non-coding RNA and long non-coding RNA
With the rapid development of RNA sequencing technology and computational methods, Long non-coding RNA (lncRNA) has been gradually recognized by researchers. lncRNA is widely distributed among animals, plants, yeasts, and even viruses, and we know that lncRNA can be involved in X chromosome silencing, genomic imprinting, chromatin modification, transcriptional activation, transcriptional interference, epigenetic regulation, and other important regulatory processes.[2]
LncRNA, known as long intergenic ncRNA or lincRNA, which is produced by the transcription of spacer sequences between genes encoded in the genome), intron long-chain non-coding RNA, sense long-chain non-coding RNA, antisense longchain non-coding RNA, and bidirectional long-chain non-coding RNA (Table 2).[8,9]
Summary
Long Non-coding RNAs, Novel Culprits, or Bodyguards in Neurodegenerative Diseases. Ding-Qi Wang,[1,7] Peng Fu,[2,7] Chengye Yao,[3,7] Ling-Shuang Zhu,[1] Tong-Yao Hou,[1] Jian-Guo Chen,[4] Youming Lu,[5] Dan Liu,[5,6] and Ling-Qiang Zhu[1,5]. LncRNA is widely distributed among animals, plants, yeasts, and even viruses, and we know that lncRNA can be involved in X chromosome silencing, genomic imprinting, chromatin modification, transcriptional activation, transcriptional interference, epigenetic regulation, and other important regulatory processes.[2]. These molecules are related to cell proliferation and differentiation, metabolism, and other physiological processes, as well as various pathological processes. MEG3 ABHD11-AS1 NaPINK1 a transcript of DiGeorge critical region 5 the human homolog of the mouse maternally expressed gene Gtl[2], the first imprinted gene identified on the mouse distal chromosome 12 homologous with rodent Abhd11os lncRNA transcribed from the antisense of PINK1 locus
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