ArticleMedical oncology (Northwood, London, England)2022
Exploring the inverse association of glioblastoma multiforme and Alzheimer's disease via bioinformatics analysis.
Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
The trial behind it
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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Unwinding the Neurovascular Unit: The Vascular Extracellular Matrix and Mechanochemical Collagen Functionalization in Vascular Dementia.International journal of molecular sciences · 2026Review
- Computational Modelling and Clinical Validation of an Alzheimer's-Related Network in Brain Cancer: The SKM034 Model.Current issues in molecular biology · 2026Article
- Article
- Deciphering novel mitochondrial signatures: multi-omics analysis uncovers cross-disease markers and oligodendrocyte pathways in Alzheimer's disease and glioblastoma.Frontiers in aging neuroscience · 2025Article
- Pericytes Are Immunoregulatory Cells in Glioma Genesis and Progression.International journal of molecular sciences · 2024Review
- A review and analysis of key biomarkers in Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Comparative Insight into Microglia/Macrophages-Associated Pathways in Glioblastoma and Alzheimer's Disease.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM) and Alzheimer's disease (AD) are two major diseases in the nervous system with a similar peak age of onset, which has the typical characteristics of high cost, difficult treatment, and poor prognosis. Epidemiological studies and a few molecular biological studies have hinted at an opposite relationship between AD and GBM. However, there are few studies on their reverse relationship, and the regulatory mechanism is still unclear, indicating that further systematic research is urgently needed. Our study firstly employs advanced bioinformatics methods to explore the inverse relationship between them and find various target drugs. We obtained the gene expression dataset from public databases (GEO, TCGA, and GTEx). Then, we identified 122 differentially expressed genes (DEGs) of AD and GBM. Four significant gene modules were identified through protein-protein interaction (PPI) and module construction, and 13 hub genes were found using cytoHubba. We constructed co-expression networks and found various target drugs through these hub genes. Functional enrichment analysis revealed that the AMPK pathway, cell cycle, and cellular senescence play important roles in AD and GBM. Our study may provide a potential direction for studying the opposite molecular mechanism of AD and GBM in the future.
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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 OpenQuestion graph.