Shared gene signatures and biochemical regulatory networks linking Parkinson's disease and ulcerative colitis.

Research overview

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Epidemiological studies suggest an association between Parkinson's disease (PD) and ulcerative colitis (UC), yet the molecular programs potentially linking these disorders remain poorly defined. Here, we integrated curated disease-gene resources with publicly available blood transcriptomic datasets to identify shared molecular features across PD and UC. We identified 320 shared signature genes and a topology-derived 10-gene core module that included TNF, IL1B, TP53, BCL2, and CASP3. Enrichment analyses implicated a convergent inflammatory-stress architecture characterized by microbial-response, oxidative-stress, lipid/inflammatory, and IL-17-related signaling programs. Immune deconvolution revealed partially overlapping peripheral immune alterations in PD and UC, most notably reduced memory B-cell abundance. Network analyses further highlighted TP53 and JUN as major transcriptional hubs and prioritized several candidate compounds for follow-up investigation. Cross-validation and external validation showed that only a subset of the core genes retained stable discriminatory performance across cohorts, indicating that network centrality did not uniformly translate into robust classifier-like behavior. Collectively, these findings support a shared inflammatory/apoptotic regulatory module linking PD and UC and provide a systems-level framework for mechanistic studies and therapeutic prioritization, rather than a definitive biomarker panel.

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