lncRNA NEAT1: Key player in neurodegenerative diseases

被引:54
作者
Li, Kun [1 ,2 ]
Wang, Ziqiang [1 ,2 ,3 ,4 ]
机构
[1] Shandong First Med Univ, Affiliated Hosp 1, Dept Nucl Med, Jinan 250014, Peoples R China
[2] Shandong Prov Qianfoshan Hosp, Jinan 250014, Peoples R China
[3] Shandong First Med Univ & Shandong Acad Med Sci, Biomed Sci Coll, Jinan 250062, Peoples R China
[4] Shandong First Med Univ & Shandong Acad Med Sci, Shandong Med Biotechnol Ctr, Jinan 250062, Peoples R China
基金
中国国家自然科学基金;
关键词
lncRNA; NEAT1; Neurodegenerative disease; Therapeutic target; Gene regulation; NONCODING RNA NEAT1; AMYOTROPHIC-LATERAL-SCLEROSIS; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; PROMOTES AUTOPHAGY; A-BETA; FUS; TDP-43; ALS; DEGRADATION;
D O I
10.1016/j.arr.2023.101878
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Neurodegenerative diseases are the most common causes of disability worldwide. Given their high prevalence, devastating symptoms, and lack of definitive diagnostic tests, there is an urgent need to identify potential bio-markers and new therapeutic targets. Long non-coding RNAs (lncRNAs) have recently emerged as powerful regulatory molecules in neurodegenerative diseases. Among them, lncRNA nuclear paraspeckle assembly tran-script 1 (NEAT1) has been reported to be upregulated in Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). However, whether this is part of a protective or harmful mechanism is still unclear. This review summarizes our current knowledge of the role of NEAT1 in neurodegenerative diseases and its association with the characteristic aggregation of misfolded proteins: amy-loid-beta and tau in AD, alpha-synuclein in PD, mutant huntingtin in HD, and TAR DNA-binding protein-43 fused in sarcoma/translocated in liposarcoma in ALS. The aim of this review is to stimulate further research on more precise and effective treatments for neurodegenerative diseases.
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页数:8
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