Shared gene signatures and biochemical regulatory networks linking Parkinson’s disease and ulcerative colitis
(2026) In npj Parkinson's Disease 12(1).- Abstract
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... (More)
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.
(Less)
- author
- Sun, Xiaohui ; An, Zhichen ; Wang, Shufei and Wang, Kongjia LU
- organization
- publishing date
- 2026-12
- type
- Contribution to journal
- publication status
- published
- subject
- in
- npj Parkinson's Disease
- volume
- 12
- issue
- 1
- article number
- 109
- publisher
- Springer Nature
- external identifiers
-
- pmid:42091906
- scopus:105038776956
- ISSN
- 2373-8057
- DOI
- 10.1038/s41531-026-01374-z
- language
- English
- LU publication?
- yes
- id
- e539ed2a-70f9-4d37-a547-9b1bc06bb64e
- date added to LUP
- 2026-08-17 11:22:22
- date last changed
- 2026-10-27 14:11:15
@article{e539ed2a-70f9-4d37-a547-9b1bc06bb64e,
abstract = {{<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 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.</p>}},
author = {{Sun, Xiaohui and An, Zhichen and Wang, Shufei and Wang, Kongjia}},
issn = {{2373-8057}},
language = {{eng}},
number = {{1}},
publisher = {{Springer Nature}},
series = {{npj Parkinson's Disease}},
title = {{Shared gene signatures and biochemical regulatory networks linking Parkinson’s disease and ulcerative colitis}},
url = {{http://dx.doi.org/10.1038/s41531-026-01374-z}},
doi = {{10.1038/s41531-026-01374-z}},
volume = {{12}},
year = {{2026}},
}