ArticleHua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology2024
Potential correlation between chronic periodontitis and Parkinson's disease.
Article in Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThis study aims to investigate possible hub genes, associated pathways, and transcription factors between chronic periodontitis (CP) and Parkinson's disease (PD).
methodsGene expression profiles of CP (GSE16134, GSE23586, and GSE10334) and PD (GSE20141 and GSE49036) were downloaded from the gene expression omnibus (GEO) database for differential expression analysis and functional clustering analysis. The protein-protein interaction (PPI) network was constructed, and hub genes were screened by four topological analysis algorithms and modular segmentation. Functional clustering analysis was performed. The hub genes were validated by external datasets of CP and PD, and causal relation was further assessed by Mendelian randomization (MR).
resultsAfter merging the data, 1 211 differentially expressed genes (DEGs) were screened in the CP datasets; of which, 551 were upregulated and 660 were downregulated. A total of 2 407 DEGs were screened in the PD dataset, of which, 1 438 were upregulated and 969 were downregulated. The PPI network included 145 nodes and 126 edges. Four hub genes (FCGR3B, PRF1, IL18, and CD33) and three transcription factors (HSF1, HSF2, and HSF4) were finally screened. The relevant pathway was predominantly natural killer (NK) cell-mediated toxic effects. The MR results suggest a possible positive causal relationship between CP and the risk of developing PD.
conclusionsThis study indicated the probably shared pathophysiology and possible causal relationship between CP and PD and may offer novel concepts and therapeutic targets for future mechanistic investigations.
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Registered trials
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