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Analysis of complement system and its related factors in Alzheimer's disease

Alzheimer's disease (AD) is a primary cause of dementia. The complement system is closely related to AD pathology and may be a potential target for the prevention and treatment of AD. In our study, we conducted a bioinformatics analysis to analyze the role of the complement system and its relat...

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Bibliographic Details
Published in:BMC neurology 2023-12, Vol.23 (1), p.446-446, Article 446
Main Authors: Zhu, Xi-Chen, Tang, Bin-Feng, Zhu, Meng-Zhuo, Lu, Jing, Lin, Han-Xiao, Tang, Jia-Ming, Li, Rong, Ma, Tao
Format: Article
Language:English
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Summary:Alzheimer's disease (AD) is a primary cause of dementia. The complement system is closely related to AD pathology and may be a potential target for the prevention and treatment of AD. In our study, we conducted a bioinformatics analysis to analyze the role of the complement system and its related factors in AD using Gene Expression Omnibus (GEO) data. We also conducted a functional analysis. Our study verified that 23 genes were closely related to differentially expressed complement system genes in diseases after intersecting the disease-related complement system module genes and differentially expressed genes. The STRING database was used to predict the interactions between the modular gene proteins of the differential complement system. A total of 21 gene proteins and 44 interaction pairs showed close interactions. We screened key genes and created a diagnostic model. The predictive effect of the model was constructed using GSE5281 and our study indicated that the predictive effect of the model was good. Our study also showed enriched negative regulation of Notch signaling, cytokine secretion involved in the immune response pathway, and cytokine secretion involved in immune response hormone-mediated apoptotic signaling pathway. We hope that our study provides a promising target to prevent and delay the onset, diagnosis, and treatment of AD.
ISSN:1471-2377
1471-2377
DOI:10.1186/s12883-023-03503-0