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<p>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 <i>TNF,</i> <i>IL1B,</i> <i>TP53</i>, <i>BCL2</i>, and <i>CASP3</i>. 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.</p>

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月6日

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  • Xiaohui Sun,
  • Zhichen An,
  • Shufei Wang,
  • Kongjia Wang

摘要

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.