ArticleBrain and behavior2026
Exploring the Causal Links Between Toxoplasma gondii Infection and Risk of Brain Tumors: A Bidirectional Mendelian Randomization Analysis.
Article in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundToxoplasma gondii (T. gondii) is a ubiquitous protozoan parasite capable of establishing lifelong latent infections in the central nervous system. Previous epidemiological studies have suggested a potential association between T. gondii infection and an increased risk of brain cancer, but the causal relationship remains unclear.
methodsWe conducted a bidirectional Mendelian randomization (MR) study to assess the causal relationship between T. gondii infection and brain tumor risk. Genetic instruments for T. gondii seropositivity were derived from a genome-wide association study (GWAS) in the UK Biobank, while genetic data for brain tumors were obtained from the FinnGen R12 dataset. Standard MR methods, including inverse-variance weighted (IVW), weighted median, and MR-Egger, were applied to infer causality, with generalized summary Mendelian randomization (GSMR) used for further validation. Sensitivity analyses, including heterogeneity and pleiotropy assessments, were performed to ensure robustness. Additionally, reverse MR analyses were conducted to evaluate whether brain tumors influence genetic liability to T. gondii seropositivity.
resultsOur MR analyses found no evidence of a causal relationship between genetic liability to T. gondii seropositivity, as indicated by P22 and SAG1 antibody levels, and the risk of brain tumors. Across all tumor subtypes, IVW, weighted median, MR-Egger, and GSMR analyses consistently yielded non-significant results. However, reverse MR analysis suggested that genetic liability to malignant brain tumors is associated with increased odds of T. gondii seropositivity. For P22, a strong association was observed across methods (IVW: OR = 1.234, p = 0.004; GSMR: OR = 1.228, p = 0.006). In contrast, for SAG1 the evidence was weaker, with IVW indicating a suggestive association (OR = 1.094, p = 0.048) and GSMR showing a borderline association (OR = 1.088, p = 0.052). Sensitivity analyses confirmed the robustness of these findings, with no evidence of heterogeneity or pleiotropy. No significant associations were observed for meningioma, glioblastoma, or benign brain tumors.
conclusionOur study provides no evidence for a causal relationship between genetic liability to T. gondii seropositivity and brain tumor risk. However, reverse MR suggests that genetic liability to malignant brain tumors may be associated with increased odds of T. gondii infection.
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.