ArticleMolecular neurobiology2024
Personalized Protein-Protein Interaction Networks Towards Unraveling the Molecular Mechanisms of Alzheimer's Disease.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- New insights into translational research in Alzheimer's disease guided by artificial intelligence, computational and systems biology.Acta pharmaceutica Sinica. B · 2025Review
- A personalized metabolic modelling approach through integrated analysis of RNA-Seq-based genomic variants and gene expression levels in Alzheimer's disease.Communications biology · 2025Article
- A benchmark of RNA-seq data normalization methods for transcriptome mapping on human genome-scale metabolic networks.NPJ systems biology and applications · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Alzheimer's disease (AD) is a highly heterogenous neurodegenerative disease, and several omic-based datasets were generated in the last decade from the patients with the disease. However, the vast majority of studies evaluate these datasets in bulk by considering all the patients as a single group, which obscures the molecular differences resulting from the heterogeneous nature of the disease. In this study, we adopted a personalized approach and analyzed the transcriptome data from 403 patients individually by mapping the data on a human protein-protein interaction network. Patient-specific subnetworks were discovered and analyzed in terms of the genes in the subnetworks, enriched functional terms, and known AD genes. We identified several affected pathways that could not be captured by the bulk comparison. We also showed that our personalized findings point to patterns of alterations consistent with the recently suggested AD subtypes.
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