Integrative bibliometric and transcriptomic analyses identify selenium-associated molecular signatures in the aging brain.
Overview
- Department of Geriatrics, Tianjin Medical University General Hospital, Tianjin, China
- Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China
- Department of Gastroenterology, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi, China
- School of Medicine, Nankai University, Tianjin, China
Abstract
Background and purpose: The aging brain is particularly sensitive to alterations in selenium status. Selenium deficiency has been associated with impaired neural function, cognitive decline, and increased vulnerability to neurodegeneration. However, the molecular mechanisms that link selenium biology to brain aging remain poorly understood.
Methods: We conducted a bibliometric analysis of 1,826 publications and identified brain-aging DEGs from public datasets. After intersecting these with selenium-related gene sets, we used machine-learning feature selection and SHAP/
Results: Bibliometric analysis showed a steady increase in publications on selenium and aging over the past two decades, with major research hotspots focusing on oxidative stress, selenoproteins, and cognitive function, while the selenium-cognition relationship remains relatively underexplored. Intersection analysis identified seven potential targets linking selenium to brain aging, from which machine-learning feature selection prioritized three core genes (SP1, SEPHS2, and MSRB1) that were significantly differentially expressed in aged samples. SHAP and nomogram analyses indicated that SP1 and SEPHS2 were the main contributors to model discrimination. Animal experiments further confirmed increased SP1 and decreased SEPHS2 expression at both mRNA and protein levels in aged mouse brains, consistent with the bioinformatic findings.
Conclusion: This study identifies SP1 and SEPHS2 as key genes linking selenium to brain aging, providing new insights into the role of selenium in brain aging and suggesting that these genes may represent potential biomarkers or therapeutic targets for brain aging and aging-related brain disorders.
Reproduced under the paper's license (CC BY), from the paper cited above.
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Data
Data links
- ncbi.nlm.nih.gov/
geo , NCBI; found in “Data availability statement”
Data availability statement
The datasets presented in this study can be found in online repositories. The repository name and accession numbers are as follows: Gene Expression Omnibus (GEO), https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
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Version 1, 28 September 2026: the first record
Recorded: type, language, journal, volume, pages, dates, 8 authors, 6 keywords, 51 references.
Cite
This paper
Liu, S., Yan, B., Gao, H., Zhang, L., Zhang, Z., Liu, Y., Chen, F., & Lei, P. (2026). Integrative bibliometric and transcriptomic analyses identify selenium-associated molecular signatures in the aging brain. Frontiers in aging neuroscience, 18, 1791352. https://
BibTeX
@article{liu2026integrat
author = {Liu, Shan and Yan, Bo and Gao, Han and Zhang, Lin and Zhang, Zihan and Liu, Yaru and Chen, Fanglian and Lei, Ping},
title = {{Integrative bibliometric and transcriptomic analyses identify selenium-associated molecular signatures in the aging brain}},
journal = {Frontiers in aging neuroscience},
year = {2026},
month = may,
volume = {18},
pages = {1791352},
publisher = {Frontiers Media SA},
issn = {1663-4365},
doi = {10.3389/
url = {https://
pmid = {42157858},
pmcid = {PMC13180909}
}
RIS
TY - JOUR
AU - Liu, Shan
AU - Yan, Bo
AU - Gao, Han
AU - Zhang, Lin
AU - Zhang, Zihan
AU - Liu, Yaru
AU - Chen, Fanglian
AU - Lei, Ping
TI - Integrative bibliometric and transcriptomic analyses identify selenium-associated molecular signatures in the aging brain
T2 - Frontiers in aging neuroscience
J2 - Front Aging Neurosci
PY - 2026
DA - 2026/
VL - 18
SP - 1791352
SN - 1663-4365
PB - Frontiers Media SA
DO - 10.3389/
UR - https://
LA - en
ER -
CSL-JSON
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