ArticleFrontiers in aging neuroscience2022
Identifying crosstalk genetic biomarkers linking a neurodegenerative disease, Parkinson's disease, and periodontitis using integrated bioinformatics analyses.
Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Identifying omic biomarkers for chronic inflammatory diseases associated with periodontitis using percolation on multi-disease gene co-expression networks.Communications medicine · 2026Article
- Salivary AQP9 mRNA expression is associated with caries and periodontitis prevalence.Scientific reports · 2026Observational
- Role of regulatory immune cells in pathogenesis and therapy of periodontitis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Role of HbA1c in Parkinson's Disease: An Integrative Analysis by Single-Cell, Bulk Transcriptome and Mendelian Randomization.Molecular neurobiology · 2025Article
- The Interplay Between Epilepsy and Parkinson's Disease: Gene Expression Profiling and Functional Analysis.Molecular biotechnology · 2025Article
- Impact of Mast Cell Activation on Neurodegeneration: A Potential Role for Gut-Brain Axis andNeurology international · 2024Review
- Exosomal mRNA Signatures as Predictive Biomarkers for Risk and Age of Onset in Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Causal role of myeloid cells in Parkinson's disease: Mendelian randomization study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Review
- Autophagy-related gene model as a novel risk factor for schizophrenia.Translational psychiatry · 2024Article
- Modulation of myeloid-derived suppressor cell functions by oral inflammatory diseases and important oral pathogens.Frontiers in immunology · 2024Review
- Joint-tissue integrative analysis identifies high-risk genes for Parkinson's disease.Frontiers in neuroscience · 2024Article
- Revisiting Alpha-Synuclein Pathways to Inflammation.International journal of molecular sciences · 2023Review
- Controlling the Impact ofMedicina (Kaunas, Lithuania) · 2023Article
- Article
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Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To identify the genetic linkage mechanisms underlying Parkinson's disease (PD) and periodontitis, and explore the role of immunology in the crosstalk between both these diseases. Methods: The gene expression omnibus (GEO) datasets associated with whole blood tissue of PD patients and gingival tissue of periodontitis patients were obtained. Then, differential expression analysis was performed to identify the differentially expressed genes (DEGs) deregulated in both diseases, which were defined as crosstalk genes. Inflammatory response-related genes (IRRGs) were downloaded from the MSigDB database and used for dividing case samples of both diseases into different clusters using k-means cluster analysis. Feature selection was performed using the LASSO model. Thus, the hub crosstalk genes were identified. Next, the crosstalk IRRGs were selected and Pearson correlation coefficient analysis was applied to investigate the correlation between hub crosstalk genes and hub IRRGs. Additionally, immune infiltration analysis was performed to examine the enrichment of immune cells in both diseases. The correlation between hub crosstalk genes and highly enriched immune cells was also investigated. Results: Overall, 37 crosstalk genes were found to be overlapping between the PD-associated DEGs and periodontitis-associated DEGs. Using clustering analysis, the most optimal clustering effects were obtained for periodontitis and PD when k = 2 and k = 3, respectively. Using the LASSO feature selection, five hub crosstalk genes, namely, FMNL1, MANSC1, PLAUR, RNASE6, and TCIRG1, were identified. In periodontitis, MANSC1 was negatively correlated and the other four hub crosstalk genes (FMNL1, PLAUR, RNASE6, and TCIRG1) were positively correlated with five hub IRRGs, namely, AQP9, C5AR1, CD14, CSF3R, and PLAUR. In PD, all five hub crosstalk genes were positively correlated with all five hub IRRGs. Additionally, RNASE6 was highly correlated with myeloid-derived suppressor cells (MDSCs) in periodontitis, and MANSC1 was highly correlated with plasmacytoid dendritic cells in PD. Conclusion: Five genes (i.e., FMNL1, MANSC1, PLAUR, RNASE6, and TCIRG1) were identified as crosstalk biomarkers linking PD and periodontitis. The significant correlation between these crosstalk genes and immune cells strongly suggests the involvement of immunology in linking both diseases.
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