Integrating Mendelian randomization, machine learning and retrospective clinical data: an exploratory analysis of the cross-disease association between CHB and PD, with a focus on eosinophil alterations.

The supplementary regression results demonstrated that the priority cross-disease genes exhibited significant or marginally significant associations with eosinophil infiltration status in the full-sample logistic regression ( RTN3 : p = 0.015; MAP4K3 : p = 0.062, marginally significant), while neither gene reached a statistically significant correlation in the beta regression restricted to non-zero eosinophil samples ( RTN3 : p = 0.056, marginally significant; MAP4K3 : p = 0.149).

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GSEA revealed trends in amino acid metabolism: GSEA of RTN3 in PD showed upregulation of glycine, serine and threonine metabolism ( Supplementary Figure S2c ); GSEA of MAP4K3 showed near-significant enrichment of phenylalanine metabolism in both PD (normalized enrichment score [NES] = −1.40, p = 0.049) and CHB (NES = 1.34, p = 0.09), with opposite enrichment directions ( Supplementary Figure S2e,f ).

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Notably, a distinct threshold effect was observed in the high CHB activity group: only the top two quartiles of eosinophil count were significantly associated with PD risk, with OR values increasing exponentially (Q3: OR = 3.65, Q4: OR = 8.39), while the second quartile did not reach statistical significance (OR = 1.92, 95%CI: 0.74–4.86, p = 0.169).

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