ArticleMolecular neurobiology2025
Mendelian Randomization in Conjunction with WGCNA Was Employed to Investigate the Potential Role of the Liver-Brain Axis in the Pathogenesis of Hepatocellular Carcinoma and Alzheimer's Disease.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Bisphenol A promotes esophageal carcinogenesis by activating the MMP1-PCOLCE regulatory axis and remodeling the tumor immune microenvironment.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Alzheimer's disease (AD) and hepatocellular carcinoma (HCC) are prevalent age-related diseases. While the gut-liver-brain axis is recognized, the molecular links between liver dysfunction and neurodegeneration in AD and HCC remain unclear. This study investigated shared dysregulated genes and pathways in AD and HCC, focusing on the liver-brain axis and potential therapeutic targets. We used combined in silico and in vivo approaches. Gene expression datasets (GEO) for AD and HCC were analyzed using DEG analysis and WGCNA to identify co-expressed modules and DEGs. Shared disease-associated genes were identified using CTD and GeneCards. Enrichment analysis (KEGG, GO) elucidated functions. PPI networks and miRTarBase identified hub genes and regulatory miRNAs. Mendelian randomization assessed shared genetic risk factors. qRT-PCR and immunohistochemistry validated findings in brain (hippocampus, prefrontal cortex) and liver tissues from AD and HCC mouse models. IL-6, MMP9, TGFB1, HSP90AA1, and STAT3 were identified as key shared genes in AD and HCC, implicating them in neuroinflammation and tumor progression. Enrichment analysis highlighted shared inflammatory pathways, including TGF-β and PI3K-Akt. has-mir-29b-3p potentially plays a role in both diseases. Mendelian randomization identified CD28-CD25 + + CD8 + T cells as a shared genetic risk factor. Increased expression of IL-6, MMP9, and STAT3 was confirmed in AD mouse brains and HCC mouse livers. This study reveals shared inflammatory mechanisms in AD and HCC, centered on key hub genes, potentially modulated by the vagus nerve. These findings inform further investigation of therapeutic targets.
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Identifiers
40858976What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.