ArticleFrontiers in neurology2020
The Predicted Key Molecules, Functions, and Pathways That Bridge Mild Cognitive Impairment (MCI) and Alzheimer's Disease (AD).
Article in Frontiers in neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it.
- MicroRNAs signatures as potential molecular markers in mild cognitive impairment: a meta-analysis.Frontiers in aging neuroscience · 2024Pooled it
- Deep Plasma Proteomics-Based Diagnostic Panel for Early Detection of Amnestic Mild Cognitive Impairment.Journal of proteome research · 2026Article
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- Cell-type-aware transcriptome-wide association studies identify 91 independent risk genes for Alzheimer's disease dementia.Communications biology · 2026Article
- Locus- and Gene-Level Insights into the Inverse Association Between Alzheimer's Disease and Cancer.International journal of molecular sciences · 2026Article
- Plasma S100 Calcium-Binding Protein A8/A9 and Cognitive Impairment After Acute Ischemic Stroke.Journal of the American Heart Association · 2026Article
- Dual Targeting of Mutant p53 and SNRPD2 via Engineered Exosomes Modulates Alternative Splicing to Suppress Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- APOE4-driven T cell dysregulation in Alzheimer's disease: single-cell genomics and Mendelian randomization reveal novel therapeutic targets.Journal of neuroinflammation · 2026Article
- From correlation to causation: cell-type-specific gene regulatory networks in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- Prefoldin 5 is a microtubule-associated protein that suppresses Tau aggregation and neurotoxicity.eLife · 2026Article
- From Correlation to Causation: Cell-Type-Specific Gene Regulatory Networks in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- Translational disease modeling of peripheral blood identifies type 2 diabetes biomarkers predictive of Alzheimer's disease.NPJ systems biology and applications · 2025Article
- Newer Therapeutic Approaches in Treating Alzheimer's Disease: A Comprehensive Review.ACS omega · 2025Review
- Pro-inflammatory S100A8 Protein Exhibits a Detergent-like Effect on Anionic Lipid Bilayers, as Imaged by High-Speed AFM.ACS applied materials & interfaces · 2025Article
- TGF-β2 Induces Ribosome Activity, Alters Ribosome Composition and Inhibits IRES-Mediated Translation in Chondrocytes.International journal of molecular sciences · 2024Article
- Fatty acid-binding protein 5 is a functional biomarker and indicator of ferroptosis in cerebral hypoxia.Cell death & disease · 2024Article
- Transcriptome- and proteome-wide effects of a circular RNA encompassing four early exons of the spinal muscular atrophy genes.Research square · 2024Article
- Consistent genes associated with structural changes in clinical Alzheimer's disease spectrum.Frontiers in neuroscience · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To elucidate the key molecules, functions, and pathways that bridge mild cognitive impairment (MCI) and Alzheimer's disease (AD), we investigated open gene expression data sets. Differential gene expression profiles were analyzed and combined with potential MCI- and AD-related gene expression profiles in public databases. Then, weighted gene co-expression network analysis was performed to identify the gene co-expression modules. One module was significantly negatively associated with MCI samples, in which gene ontology function and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed that these genes were related to cytosolic ribosome, ribosomal structure, oxidative phosphorylation, AD, and metabolic pathway. The other two modules correlated significantly with AD samples, in which functional and pathway enrichment analysis revealed strong relationships of these genes with cytoplasmic ribosome, protein binding, AD, cancer, and apoptosis. In addition, we regarded the core genes in the module network closely related to MCI and AD as bridge genes and submitted them to protein interaction network analysis to screen for major pathogenic genes according to the connectivity information. Among them, small nuclear ribonucleoprotein D2 polypeptide (
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