Decoding Dementia Mechanisms: Identification of Key Oligodendrocyte Associated Genes through Integrative Bioinformatics and MachineLearning

小桶 基因 痴呆 免疫系统 计算生物学 基因表达 生物信息学 生物 遗传学 医学 基因本体论 疾病 病理
作者
Yan Chen,Hao Wen,Xinyi Qiu,Chen Li,Yinhui Yao,Shang Yazhen
出处
期刊:Current Topics in Medicinal Chemistry [Bentham Science Publishers]
卷期号:25
标识
DOI:10.2174/0115680266384153250804110312
摘要

INTRODUCTION: This study aims to elucidate the mechanisms underlying Dementia using bioinformatics analysis and machine learning algorithms, to identify novel therapeutic targets for its clinical management. METHODS: Gene expression datasets related to dementia were sourced from the GEO database. Differentially expressed genes (DEGs) were identified using R, and key module genes were determined through the Weighted Gene Co-expression Network Analysis (WGCNA) method. Oligodendrocyte (OL) related targets were retrieved from the GeneCards database. The intersecting genes from DEGs, WGCNA, and OL were analyzed using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes. Subsequently, three machine learning algorithms were employed to pinpoint core genes associated with OL in dementia. The CIBERSORT algorithm was used to evaluate the abundance of 22 immune cell types and their correlation with Dementia-related immune infiltration. Validation was carried out via quantitative reverse transcription polymerase chain reaction (RT-qPCR). RESULTS: Through bioinformatics and machine learning techniques, six core OL genes associated with Dementia were identified, notably C1QA, CD163, and TGFB2, which showed elevated expression in Dementia. Immune cell infiltration analysis indicated that several immune cell types may contribute to Dementia's pathogenesis, and RT-qPCR results corroborated the bioinformatics findings. DISCUSSION: The discovered genes may contribute to dementia pathogenesis through oligodendrocyte dysfunction and neuroimmune interactions. Notably, TGFB2 and complement-related genes (C1QA, CD163) suggest involvement in both myelination defects and neuroinflammation, highlighting their therapeutic potential. CONCLUSION: The six feature genes: TGFB2, C1QA, CD163, ACTG1, WIF1, and OPALIN are significantly linked to Dementia.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
朝气完成签到,获得积分10
刚刚
楠楠完成签到,获得积分10
1秒前
华仔应助Dlan采纳,获得10
1秒前
1秒前
章半仙完成签到,获得积分10
1秒前
龙少在612完成签到,获得积分10
1秒前
2秒前
2秒前
Beagle发布了新的文献求助10
3秒前
7788999完成签到,获得积分10
3秒前
熊若宇发布了新的文献求助10
3秒前
闪闪的从安完成签到,获得积分10
5秒前
卖艺的读书人完成签到 ,获得积分10
6秒前
lala完成签到,获得积分10
6秒前
chen发布了新的文献求助10
6秒前
ly发布了新的文献求助10
6秒前
Freeasy发布了新的文献求助10
7秒前
时尚初柳完成签到,获得积分10
7秒前
lalala应助supersuper采纳,获得10
7秒前
103x发布了新的文献求助20
7秒前
ww完成签到,获得积分10
8秒前
cc2941完成签到,获得积分10
9秒前
9秒前
完美世界应助不朽丶哀默采纳,获得10
10秒前
瑶625完成签到,获得积分10
10秒前
许琦完成签到,获得积分10
10秒前
哈哈哈哈应助小巧采白采纳,获得40
10秒前
anyuezou完成签到,获得积分10
11秒前
SciGPT应助Yummy采纳,获得10
11秒前
hhyhjhj发布了新的文献求助10
11秒前
zhang完成签到,获得积分20
12秒前
光头强完成签到,获得积分10
12秒前
莫愁完成签到,获得积分10
12秒前
翁雁丝完成签到 ,获得积分10
12秒前
zsl完成签到,获得积分10
13秒前
iNk应助重若轻111采纳,获得30
13秒前
13秒前
熊若宇完成签到,获得积分10
13秒前
乾雨完成签到 ,获得积分10
13秒前
zhuzhu完成签到 ,获得积分10
13秒前
高分求助中
Clinical Epidemiology: The Essentials, 6e 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
The Graphene Handbook (2019 Edition) 800
Adhesion Science: Principles & Practice 800
Signals, Systems, and Signal Processing 610
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 600
久松真一著作集〈第5巻〉禅と芸術 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6556249
求助须知:如何正确求助?哪些是违规求助? 8340289
关于积分的说明 17868629
捐赠科研通 5674562
什么是DOI,文献DOI怎么找? 2940515
邀请新用户注册赠送积分活动 1916404
关于科研通互助平台的介绍 1786997