Exploring the inverse association of glioblastoma multiforme and Alzheimer’s disease via bioinformatics analysis

Cai, Jiayang; Ye, Liguo; Hu, Yuanyuan; Ye, Zhang; Gao, Lun; Wang, Yixuan; Sun, Qian; Tong, Shiao; Yang, Jian; Chen, Qianxue

doi:10.1007/s12032-022-01786-w

Cited by 8 publications

(7 citation statements)

References 40 publications

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“…Indeed, AD and GBM seem to be in opposite semiplanes. Clinical evidence [3,4,5,6] and molecular biology studies [7,8,9] support this disjunctive. Consequently, the PC2 axis involve genes inversely deregulated in AD and GBM.…”

Section: Resultsmentioning

confidence: 99%

“…The plot shows that aging is a common risk factor for GBM and AD and, at the same time, that GBM and AD are opposite alternatives, as epidemiological [3,4,5,6] and molecular biology studies [7,8,9] suggest. The plot indicates also a path or corridor for normal aging, in accordance with the programmatic aging theory [10,11].…”

Section: Introductionmentioning

confidence: 99%

“…We provide a drawing for white matter of the brain in which the normal state is represented along with the glioblastoma (GBM) attractor and the seemingly modest maximum related to Alzheimer disease (AD). The plot shows that GBM and AD are opposite alternatives, as epidemiological [3,4,5,6] and molecular biology studies [7,8,9] suggest, and indicates a path or corridor for normal aging, in accordance with the programmatic aging theory [10,11]. At the gene level, there are genes varying in the same way in the aging, AD progression and cancer processes, whereas there are also genes indicating the disjunctive between AD and GBM.…”

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confidence: 99%

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A bird’s eye view to the homeostatic, Alzheimer and Glioblastoma attractors

Nieves,

Gil,

Gonzalez

2023

Preprint

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A well known paradigm in molecular genetics expresses that local maxima of fitness in gene expression space are related to biological viable states [1]. This picture has been applied to the description of cell fates along differentiation lines [2]. However, to the best of our knowledge, there are no plots based on real data for a given tissue representing at least a partial landscape with more than two of these maxima. We provide a drawing for white matter of the brain in which the normal state is represented along with the glioblastoma (GBM) attractor and the seemingly modest maximum related to Alzheimer disease (AD). The plot shows that GBM and AD are opposite alternatives, as epidemiological [3,4,5,6] and molecular biology studies [7,8,9] suggest, and indicates a path or corridor for normal aging, in accordance with the programmatic aging theory [10,11]. At the gene level, there are genes varying in the same way in the aging, AD progression and cancer processes, whereas there are also genes indicating the disjunctive between AD and GBM. An example of the latter is the MMP9 protein-coding gene, playing an important role in tumor invasion [12,13], but known also as a neuroprotector, controlling the interactions between axons and beta-amyloid fibers [14]. Deviations of the gene expression value from its reference in normal tissue may indicate either a potential progression to AD (under-expression) or to GBM (over-expression). This unusual view, following from a simple plot, may help understand the relations between AD and GBM biology and identify useful gene markers for both processes. We anticipate that similar diagrams could be important in other tissues.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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A bird’s eye view to the homeostatic, Alzheimer and Glioblastoma attractors

Nieves,

Gil,

Gonzalez

2023

Preprint

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“…Yılmaz (2020) found five genes as common DEG for five datasets of AD and cancer, EGFR for AD-breast cancer, SOX9 for AD-colorectal cancer, THBS1 for AD-lung cancer, and ‘VEGFA’ for AD-prostate cancer were identified as the most significant hub genes in network analysis. Cai J. et al (2022) screened 13 hub genes of AD and Glioblastoma multiforme by seven typical algorithms co-expression networks. miRNAs are involved in the regulation of various cellular processes including pathological conditions.…”

Section: Identification Of Shared Candidate Biomarkers Between Ad And...mentioning

confidence: 99%

A review and analysis of key biomarkers in Alzheimer’s disease

Zhang,

Liu,

Zhang

et al. 2024

Front. Neurosci.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that affects over 50 million elderly individuals worldwide. Although the pathogenesis of AD is not fully understood, based on current research, researchers are able to identify potential biomarker genes and proteins that may serve as effective targets against AD. This article aims to present a comprehensive overview of recent advances in AD biomarker identification, with highlights on the use of various algorithms, the exploration of relevant biological processes, and the investigation of shared biomarkers with co-occurring diseases. Additionally, this article includes a statistical analysis of key genes reported in the research literature, and identifies the intersection with AD-related gene sets from databases such as AlzGen, GeneCard, and DisGeNet. For these gene sets, besides enrichment analysis, protein–protein interaction (PPI) networks utilized to identify central genes among the overlapping genes. Enrichment analysis, protein interaction network analysis, and tissue-specific connectedness analysis based on GTEx database performed on multiple groups of overlapping genes. Our work has laid the foundation for a better understanding of the molecular mechanisms of AD and more accurate identification of key AD markers.

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“…Glioma and AD share aging as a common risk factor, but a number of studies suggest an inverse relationship of the two diseases. That is, older persons with cancer have a reduced risk of AD and vice versa [13][14][15]. Only a few studies have explored that AD and malignant brain tumor were positively correlated [16].…”

Section: Introductionmentioning

confidence: 99%

Mendelian randomization study on the causal effects of glioma on Alzheimer's disease

Zhang

Zeng

Zhu

et al. 2023

Preprint

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Background Previous observational studies have revealed an inverse relationship where cancer patients have a reduced risk to develop Alzheimer’s disease (AD) and vice versa. The present two-sample Mendelian randomization (MR) study aims to identify the causal link between gliomas and AD. Methods The largest gliomas genome-wide association study (GWAS) was used. A previously reported AD GWAS (24,087 cases and 55,058 controls from European ancestry) was used to assess the effect of gliomas on AD. MR-egger_intercept and MR_egger and inverse variance weighted (IVW) in Cochran’s Q-test were used to determine the pleiotropy and heterogeneity, respectively. IVW and weighted median were used to perform MR analysis. Finally, the effect of a single nucleotide polymorphism (SNP) was used to test the SNP bias. Results We did not find a significant pleiotropy or heterogeneity of all three gliomas genetic instrumental variants (IVs) in AD GWAS. Interestingly, we found that as gliomas genetically increased, the risk of AD increased using IVW (odds ratio [OR] = 1.0167, 95% confidence interval [CI] = 1.0079–1.0257, p = 0.0002). This was further proven by weighted median (OR = 1.0161, 95% CI = 1.0058–1.0267, p = 0.0023). Reverse MR analysis shows no causal effect of AD on gliomas. Conclusions Our analysis suggested a causal link between genetically increased gliomas and the increased risk of AD in European ancestries. Thus, gliomas may be a risk factor for AD.

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Exploring the inverse association of glioblastoma multiforme and Alzheimer’s disease via bioinformatics analysis

Cited by 8 publications

References 40 publications

A bird’s eye view to the homeostatic, Alzheimer and Glioblastoma attractors

A bird’s eye view to the homeostatic, Alzheimer and Glioblastoma attractors

A review and analysis of key biomarkers in Alzheimer’s disease

Mendelian randomization study on the causal effects of glioma on Alzheimer's disease

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