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Case-control study shows no link between Toxoplasma gondii infection and Parkinson’s disease severity, suggesting reconsideration of neurodegeneration pathways.
Toxoplasma gondii infects nearly one-third of the global population and has been implicated in neurologic dysfunction; however, its contribution to Parkinson’s disease (PD) remains unresolved. Here we assess whether T. gondii seropositivity is associated with PD occurrence or severity in a well-defined group of patients and matched controls. A case–control design included n = 60 PD patients and n = 60 matched controls, with anti- T. gondii IgG/IgM quantified by ELISA and PD severity graded using the Hoehn and Yahr scale. Logistic regression evaluated associations ( P < 0.05). Among 120 participants (60 PD, 60 controls; mean age 69.7 ± 9.0 years; 66.7% male), education differed significantly (illiteracy: 58.3% vs. 30.0%, p < 0.001). Risk factors for T. gondii infection showed no significant differences: cat contact (61.7% vs. 56.7%; OR = 1.22, 95% CI: 0.57–2.62), unwashed vegetables (20.0% vs. 21.7%; OR = 0.90, 95% CI: 0.36–2.25), and undercooked meat (15.0% vs. 16.7%; OR = 0.88, 95% CI: 0.30–2.57). Overall IgG seroprevalence was 90.8% (PD 88.3%, controls 93.3%; adjusted OR = 0.56, 95% CI: 0.16–1.94, p = 0.36). IgG positivity did not vary significantly by PD severity (85.7–100% across Hoehn and Yahr stages), and only one PD patient was IgM-positive. The data establish that chronic T. gondii exposure does not differentiate PD patients from controls and does not convincingly modulate disease severity. This work provides a new framework for interpreting parasite–neurodegeneration links in high-exposure settings and opens the door to future studies using molecular assays and longitudinal designs to resolve causal pathways.
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Davoodi et al. (2026) studied this question.
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