Noncoding RNAs in Alzheimer's disease.
Noncoding RNAs in Alzheimer's disease.
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DOI：
10.1002/wrna.1463
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发表时间：
2018-03
期刊：
影响因子：
--
通讯作者：
Gorospe M
中科院分区：
文献类型：
--
作者：
Idda ML;Munk R;Abdelmohsen K;Gorospe M
阿尔茨海默病（Alzheimer's disease，AD）是一种进行性神经退行性疾病，是世界范围内老年痴呆的主要病因。尽管大力开发用于预防和治疗AD的药物，但目前还没有有效的治疗方法，这给个人、医疗和社会经济水平带来了越来越大的负担。AD的特征在于衍生自淀粉样前体蛋白（APP）的淀粉样β（Aβ）肽的产生和聚集、过度磷酸化微管相关蛋白Tau（MAPT）的存在以及导致神经元损失的慢性炎症。Aβ积聚和过度磷酸化Tau分别是AD、Aβ斑块和神经元缠结（NFT）的主要组织病理学特征。然而，有助于AD发病机制的分子因素的全谱尚不清楚。非编码（nc）RNA包括microRNA（miRNAs）、长链非编码RNA（lncRNA）和环状RNA（circRNA），在各种疾病中在转录和转录后水平调节基因表达，作为生物标志物和潜在的治疗靶点。越来越多的人认识到ncRNA与AD的发病和发病机制有关。在这里，我们回顾了转录后参与主要AD途径的ncRNA，并讨论了越来越多的兴趣，在治疗上靶向调节ncRNA，以打击AD病理。
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the main cause of dementia among the elderly worldwide. Despite intense efforts to develop drugs for preventing and treating AD, no effective therapies are available as yet, posing a growing burden at the personal, medical, and socioeconomic levels. AD is characterized by the production and aggregation of amyloid β (Aβ) peptides derived from amyloid precursor protein (APP), the presence of hyperphosphorylated microtubule-associated protein Tau (MAPT), and chronic inflammation leading to neuronal loss. Aβ accumulation and hyperphosphorylated Tau are responsible for the main histopathological features of AD, Aβ plaques and neurofibrillary tangles (NFTs), respectively. However, the full spectrum of molecular factors that contribute to AD pathogenesis is not known. Noncoding (nc)RNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), regulate gene expression at the transcriptional and post-transcriptional levels in various diseases, serving as biomarkers and potential therapeutic targets. There is rising recognition that ncRNAs have been implicated in both the onset and pathogenesis of AD. Here, we review the ncRNAs implicated post-transcriptionally in the main AD pathways and discuss the growing interest in targeting regulatory ncRNAs therapeutically to combat AD pathology.
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