<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>2024</volume><submitter>Xue H</submitter><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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, &lt;i>P&lt;/i> = 0.027; OR: 1.18, 95%CI: 1.01-1.38, &lt;i>P&lt;/i> = 0.041; and OR: 1.23, 95%CI: 1.04-1.46, &lt;i>P&lt;/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.&lt;h4>Conclusion&lt;/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.</pubmed_abstract><journal>Journal of immunology research</journal><pagination>9069870</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10919978</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Assessing the Causal Relationship between Genetically Determined Inflammatory Cytokines and Parkinson's Disease Risk: A Bidirectional Two-Sample Mendelian Randomization Study.</pubmed_title><pmcid>PMC10919978</pmcid><pubmed_authors>Luo Q</pubmed_authors><pubmed_authors>Fan W</pubmed_authors><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Xue H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Assessing the Causal Relationship between Genetically Determined Inflammatory Cytokines and Parkinson's Disease Risk: A Bidirectional Two-Sample Mendelian Randomization Study.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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, &lt;i>P&lt;/i> = 0.027; OR: 1.18, 95%CI: 1.01-1.38, &lt;i>P&lt;/i> = 0.041; and OR: 1.23, 95%CI: 1.04-1.46, &lt;i>P&lt;/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.&lt;h4>Conclusion&lt;/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.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024</publication><modification>2025-04-04T12:34:40.958Z</modification><creation>2025-04-04T12:34:40.958Z</creation></dates><accession>S-EPMC10919978</accession><cross_references><pubmed>38455364</pubmed><doi>10.1155/2024/9069870</doi></cross_references></HashMap>