Unraveling the Intricacies: The Role of miRNAs in the Progression and Initiation of Alzheimer's Disease

Forouzan Amerizadeh, Elnaz Farzadifar
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Abstract

Aim: This study aims to investigate the molecular mechanisms underlying Alzheimer's disease (AD) by analyzing differentially expressed miRNAs and their target proteins to identify key regulatory networks and therapeutic targets.

Background: Alzheimer's disease (AD) is a complex neurodegenerative disorder with multifaceted regulatory mechanisms involving differentially expressed miRNAs. Recent studies suggest that understanding the target proteins of these miRNAs may reveal crucial insights into AD pathology.

Objective: The objective of this study was to investigate the role of differentially expressed miRNAs in Alzheimer's disease (AD) by identifying their target proteins and exploring the associated regulatory networks. This includes uncovering key hub proteins and their involvement in critical biological pathways linked to AD progression. Additionally, the study aims to identify transcription factors regulating these proteins and evaluate potential therapeutic compounds targeting these molecular players. By integrating these findings, the research seeks to provide a deeper understanding of AD pathogenesis and pave the way for novel therapeutic strategies to mitigate its progression.

Methods and materials: Differentially expressed miRNAs were collected from reviews, with target proteins identified using MiRDB, STRING, and Cytoscape. Promoter and transcription factor (TF) analyses were performed using Enrichr, and potential therapeutic compounds targeting hub proteins were explored via DrugBank.

Results: This study identifies key hub proteins, including TNF, PTEN, KRAS, ESR1, H3-3B, COL25A1, COL19A1, COL13A1, COL27A1, COL5A3, CCND1, FGF2, SMAD2, and PXDN, exploring their roles in AD progression. GO and KEGG pathway analyses revealed that hub proteins, including TNF, PTEN, KRAS, and ESR1, are involved in essential biological processes related to neural differentiation and signaling. Cytocluster analysis identified clusters with significant associations with AD, indicating complex interaction networks among these proteins.

Discussion: Potential therapeutic agents, including TNF inhibitors, estrogen receptor agonists, and KRAS inhibitors, were identified. Promoter and TF analysis further highlighted regulatory factors in AD pathways.

Conclusion: This study emphasizes crucial AD-related proteins and pathways, providing insights for future therapeutic targeting of gene expression to mitigate AD progression.

解开复杂性:mrna在阿尔茨海默病的进展和开始中的作用。
目的:本研究旨在通过分析差异表达的mirna及其靶蛋白,探索阿尔茨海默病(AD)的分子机制,以确定关键的调控网络和治疗靶点。背景:阿尔茨海默病(AD)是一种复杂的神经退行性疾病,具有涉及差异表达的mirna的多方面调节机制。最近的研究表明,了解这些mirna的靶蛋白可能揭示阿尔茨海默病病理的重要见解。目的:本研究的目的是通过鉴定其靶蛋白并探索相关的调控网络,探讨差异表达的mirna在阿尔茨海默病(AD)中的作用。这包括揭示关键枢纽蛋白及其参与与AD进展相关的关键生物学途径。此外,该研究旨在确定调节这些蛋白质的转录因子,并评估针对这些分子参与者的潜在治疗化合物。通过整合这些发现,该研究旨在为阿尔茨海默病的发病机制提供更深入的了解,并为缓解其进展的新治疗策略铺平道路。方法和材料:从综述中收集差异表达的mirna,使用MiRDB、STRING和Cytoscape鉴定靶蛋白。利用enrichment进行启动子和转录因子(TF)分析,并通过DrugBank探索靶向枢纽蛋白的潜在治疗化合物。结果:本研究确定了关键枢纽蛋白,包括TNF、PTEN、KRAS、ESR1、H3-3B、COL25A1、COL19A1、COL13A1、COL27A1、COL5A3、CCND1、FGF2、SMAD2和PXDN,探讨了它们在AD进展中的作用。GO和KEGG通路分析显示,枢纽蛋白,包括TNF、PTEN、KRAS和ESR1,参与与神经分化和信号传导相关的基本生物学过程。细胞聚类分析鉴定出与AD显著相关的聚类,表明这些蛋白之间存在复杂的相互作用网络。讨论:确定了潜在的治疗剂,包括TNF抑制剂、雌激素受体激动剂和KRAS抑制剂。启动子和TF分析进一步强调了AD通路中的调节因子。结论:该研究强调了AD相关的关键蛋白和通路,为未来的基因表达靶向治疗提供了见解,以减轻AD的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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