{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["2024"],"submitter":["Xue H"],"pubmed_abstract":["<h4>Background</h4>Observational studies have suggested an association between inflammatory cytokines and Parkinson's disease (PD). This Mendelian randomization (MR) was conducted to further assess the causal correlations between inflammatory cytokines and PD.<h4>Methods</h4>Genetic instruments associated with inflammatory cytokines were extracted from a large summary genome-wide association studies (GWAS) involving 8,293 European participants. Summary-level statistics for PD were obtained from a large-sample GWAS containing 17 studies that involved European participants. Causalities of exposures and outcomes were explored mainly using inverse variance weighted (IVW) method.<h4>Results</h4>The IVW method indicated that basic fibroblast growth factor (FGFBasic), interleukin-2 (IL-2), and macrophage migration inhibitory factor (MIF) may be suggestively associated with the risk of PD (OR: 0.71, 95%CI: 0.52-0.96, <i>P</i> = 0.027; OR: 1.18, 95%CI: 1.01-1.38, <i>P</i> = 0.041; and OR: 1.23, 95%CI: 1.04-1.46, <i>P</i> = 0.018). In the reverse direction, monokine induced by interferon gamma (MIG), beta nerve growth factor (bNGF), interleukin-17 (IL-17), and interferon gamma (IFNg) are suggested to be the consequences of PD.<h4>Conclusion</h4>Our MR analysis indicated that suggestive associations between circulating levels of FGFBasic, IL-2, and MIF and PD risk. In addition, MIG, bNGF, IL-17, and IFNg are more likely to be involved in the development of downstream PD."],"journal":["Journal of immunology research"],"pagination":["9069870"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10919978"],"repository":["biostudies-literature"],"pubmed_title":["Assessing the Causal Relationship between Genetically Determined Inflammatory Cytokines and Parkinson's Disease Risk: A Bidirectional Two-Sample Mendelian Randomization Study."],"pmcid":["PMC10919978"],"pubmed_authors":["Luo Q","Fan W","Chen J","Xue H"],"additional_accession":[]},"is_claimable":false,"name":"Assessing the Causal Relationship between Genetically Determined Inflammatory Cytokines and Parkinson's Disease Risk: A Bidirectional Two-Sample Mendelian Randomization Study.","description":"<h4>Background</h4>Observational studies have suggested an association between inflammatory cytokines and Parkinson's disease (PD). This Mendelian randomization (MR) was conducted to further assess the causal correlations between inflammatory cytokines and PD.<h4>Methods</h4>Genetic instruments associated with inflammatory cytokines were extracted from a large summary genome-wide association studies (GWAS) involving 8,293 European participants. Summary-level statistics for PD were obtained from a large-sample GWAS containing 17 studies that involved European participants. Causalities of exposures and outcomes were explored mainly using inverse variance weighted (IVW) method.<h4>Results</h4>The IVW method indicated that basic fibroblast growth factor (FGFBasic), interleukin-2 (IL-2), and macrophage migration inhibitory factor (MIF) may be suggestively associated with the risk of PD (OR: 0.71, 95%CI: 0.52-0.96, <i>P</i> = 0.027; OR: 1.18, 95%CI: 1.01-1.38, <i>P</i> = 0.041; and OR: 1.23, 95%CI: 1.04-1.46, <i>P</i> = 0.018). In the reverse direction, monokine induced by interferon gamma (MIG), beta nerve growth factor (bNGF), interleukin-17 (IL-17), and interferon gamma (IFNg) are suggested to be the consequences of PD.<h4>Conclusion</h4>Our MR analysis indicated that suggestive associations between circulating levels of FGFBasic, IL-2, and MIF and PD risk. In addition, MIG, bNGF, IL-17, and IFNg are more likely to be involved in the development of downstream PD.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2025-04-04T12:34:40.958Z","creation":"2025-04-04T12:34:40.958Z"},"accession":"S-EPMC10919978","cross_references":{"pubmed":["38455364"],"doi":["10.1155/2024/9069870"]}}