Informational Analysis and Prediction of Obsessive-Compulsive Disorder Pathogenesis

IF 1.8 4区 医学 Q3 PSYCHIATRY Psychiatry Investigation Pub Date : 2024-05-25 DOI:10.30773/pi.2023.0149
Yanrong Wang, Yuan Wang, Manxue Zhang, Doudou Liu, Jianqun Fang
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Abstract

Objective We aimed to predict the possible mechanism of obsessive-compulsive disorder (OCD) by integrating and analyzing mRNA sequencing results from two datasets and to provide direction for future studies into the pathogenesis of OCD.Methods Two OCD datasets, GSE78104 and GSE60190, were obtained, and the intersection of the two gene sets with differential expression in OCD samples was selected. Kyoto Encyclopedia of Genes and Genomes (KEGG) signal pathway enrichment and Gene Ontology (GO) analyses were performed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) online analysis website for the genes at the intersection, and the data were mapped using http://www.bioinformatics.com.cn. After genes with p≤0.05 had been screened out, protein-protein interaction (PPI) interaction analysis was conducted using Metascape to screen the key Molecular Complex Detection (MCODE) genes. MCODE genes were then enriched using the KEGG signaling pathway and GO classification.Results A total of 3,449 differentially expressed genes (DEGs) were obtained from the GSE78104 and GSE60190 datasets. KEGG, GO, and Gene Set Enrichment Analysis analyses of DEGs showed that the onset of OCD was related to oxidative phosphorylation and other metabolic processes, which may have a similar pathogenesis to other neurodegenerative diseases. Single-gene PPI analysis of SAPAP3 revealed that the mechanism by which SAPAP3 knockout induces OCD may also be caused by affecting oxidative phosphorylation.Conclusion The mechanism of SAPAP3 knockout-induced OCD in mice may be due to the oxidative phosphorylation process in the body. Future studies on the neural circuit mechanism of OCD should be conducted.
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强迫症发病机制的信息分析与预测
目的 通过整合分析两个数据集的mRNA测序结果,预测强迫症(OCD)的可能发病机制,为今后研究强迫症的发病机制提供方向。方法 获得两个强迫症数据集GSE78104和GSE60190,选择两个基因集的交叉点在强迫症样本中的差异表达。利用注释、可视化和综合发现数据库(DAVID)在线分析网站对交集处的基因进行了京都基因组百科全书(KEGG)信号通路富集和基因本体(GO)分析,并利用 http://www.bioinformatics.com.cn 对数据进行了映射。在筛选出p≤0.05的基因后,利用Metascape进行了蛋白质-蛋白质相互作用(PPI)分析,筛选出关键的分子复合体检测(MCODE)基因。结果 从 GSE78104 和 GSE60190 数据集中共获得 3,449 个差异表达基因(DEGs)。DEGs的KEGG、GO和基因组富集分析表明,强迫症的发病与氧化磷酸化和其他代谢过程有关,其发病机制可能与其他神经退行性疾病类似。SAPAP3的单基因PPI分析表明,SAPAP3基因敲除诱导强迫症的机制也可能是通过影响氧化磷酸化过程引起的。今后应继续对强迫症的神经回路机制进行研究。
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来源期刊
CiteScore
4.10
自引率
3.70%
发文量
105
审稿时长
6-12 weeks
期刊介绍: The Psychiatry Investigation is published on the 25th day of every month in English by the Korean Neuropsychiatric Association (KNPA). The Journal covers the whole range of psychiatry and neuroscience. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and management of neuropsychiatric disorders and symptoms, as well as researches related to cross cultural psychiatry and ethnic issues in psychiatry. The Journal publishes editorials, review articles, original articles, brief reports, viewpoints and correspondences. All research articles are peer reviewed. Contributions are accepted for publication on the condition that their substance has not been published or submitted for publication elsewhere. Authors submitting papers to the Journal (serially or otherwise) with a common theme or using data derived from the same sample (or a subset thereof) must send details of all relevant previous publications and simultaneous submissions. The Journal is not responsible for statements made by contributors. Material in the Journal does not necessarily reflect the views of the Editor or of the KNPA. Manuscripts accepted for publication are copy-edited to improve readability and to ensure conformity with house style.
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