ArticleCureus2026
Causal Effects Between Antibody-Mediated Immune Responses and Parkinson's Disease: Insights from Genetic Studies.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParkinson's disease (PD) is a multifactorial neurodegenerative disorder with a complex etiology. Increasing evidence suggests that antibody-mediated immune responses elicited by prior infectious exposures may contribute to its pathogenesis; however, whether these associations reflect true causal relationships remains unresolved, largely due to confounding and other inherent limitations of observational study designs. METHODOLOGY: We conducted a two-sample Mendelian randomization (MR) analysis to interrogate the causal associations between 46 antibody-mediated immune responses and PD risk, leveraging Genome-wide association study (GWAS) summary statistics for antibody-related traits and PD data from the FinnGen consortium (5,861 cases and 494,487 controls of European ancestry). Independent genetic variants reaching genome-wide significance were selected as instrumental variables. Causal estimates were primarily derived using the inverse-variance weighted approach, with complementary analyses conducted using the weighted median, MR-Egger regression, and both simple and weighted mode methods. Bayesian weighted MR, together with a series of sensitivity analyses, was employed to evaluate the robustness of the findings and interrogate potential heterogeneity and horizontal pleiotropy.
resultsAmong the 46 antibody-mediated immune responses analyzed, two showed statistically significant causal associations with PD after Bonferroni correction. Genetically predicted elevated antibody levels against Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA-1) were significantly associated with an increased risk of PD (odds ratio (OR) = 1.154, 95% confidence interval (CI): 1.098-1.214,
conclusionsThis MR study offers genetic evidence supporting a potential causal involvement of specific antibody-mediated immune responses in the pathogenesis of PD. Elevated EBNA-1 antibody levels are associated with an increased risk of PD, whereas anti-polyomavirus 2 IgG seropositivity appears to confer a protective effect. These findings provide new insights into the immunological mechanisms underlying PD and underscore the potential of immune-related biomarkers and therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.