神经退行性疾病是全球伤残最常见的原因。由于其高发病率、致命症状和缺乏明确的诊断测试，迫切需要确定潜在生物标志物和新的治疗靶点。长链非编码RNA（lncRNA）已经成为神经退行性疾病中强大的调节分子。其中，lncRNA核剪切体组装转录本1（NEAT1）已被报道在阿尔茨海默病（AD）、帕金森病（PD）、亨廷顿病（HD）和肌萎缩侧索硬化症（ALS）中上调。但是，这是否是一种保护性或有害机制还不清楚。本文综述了我们对NEAT1在神经退行性疾病中的作用及其与蛋白质错误折叠的特征性聚集物——在AD中为β-淀粉样蛋白和tau、在PD中为α-突触核蛋白、在HD中是突变的猎琴体蛋白、在ALS中是与脂肪肉瘤转位的TAR DNA结合蛋白-43融合等方面的关联。本文旨在促进对神经退行性疾病更精确和有效治疗的进一步研究。 版权所有©2023 Elsevier B.V.之作者。

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 biomarkers 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 transcript 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: amyloid-β and tau in AD, α-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.Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.