hsa-miR-132 和 hsa-miR-129 的下调：阿尔茨海默病的非编码 RNA 分子特征

IF 3.5 3区医学 Q2 NEUROSCIENCES

Frontiers in Molecular Neuroscience Pub Date : 2024-06-25 DOI:10.3389/fnmol.2024.1423340

Siranjeevi Nagaraj, Carolina Quintanilla-Sánchez, Kunie Ando, Lidia Lopez-Gutierrez, Emilie Doeraene, Andreea-Claudia Kosa, Emmanuel Aydin, Jean-Pierre Brion, Karelle Leroy

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引用次数: 0

摘要

阿尔茨海默病（AD）影响老年人群，导致记忆障碍、认知和行为异常。目前尚无根治性治疗方法，因此有必要探索改变疾病进展的治疗方案。微小RNA（miRNA）作为非编码RNA，具有多方面的靶向潜力，已知在老年痴呆症病理中存在失调。这篇微型综述将重点关注两种有前景的 miRNA，即 hsa-miR-132 和 hsa-miR-129，它们在 AD 中始终表现出不同的调控。通过采用计算预测并参考已发表的 RNA 测序数据集，我们阐明了与 hsa-miR-132 和 hsa-miR-129 相关的 miRNA-mRNA 目标之间错综复杂的关系。我们的综述一致认为，在过去 15 年的 AD 研究中，hsa-miR-132 和 hsa-miR-129 在 AD 大脑中的下调是一种非编码 RNA 分子特征。

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Downregulation of hsa-miR-132 and hsa-miR-129: non-coding RNA molecular signatures of Alzheimer’s disease

Alzheimer’s disease (AD) affects the elderly population by causing memory impairments, cognitive and behavioral abnormalities. Currently, no curative treatments exist, emphasizing the need to explore therapeutic options that modify the progression of the disease. MicroRNAs (miRNAs), as non-coding RNAs, demonstrate multifaceted targeting potential and are known to be dysregulated in AD pathology. This mini review focuses on two promising miRNAs, hsa-miR-132 and hsa-miR-129, which consistently exhibit differential regulation in AD. By employing computational predictions and referencing published RNA sequencing dataset, we elucidate the intricate miRNA-mRNA target relationships associated with hsa-miR-132 and hsa-miR-129. Our review consistently identifies the downregulation of hsa-miR-132 and hsa-miR-129 in AD brains as a non-coding RNA molecular signature across studies conducted over the past 15 years in AD research.

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来源期刊

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.