Evidence map›Paper›PMID 40778305›Full record

ArticleFrontiers in aging neuroscience2025

Estimating progression of Alzheimer's disease with extracellular vesicle-related multi-omics risk models.

Xiao Zhang, Sanoji Wijenayake, Shakhawat Hossain, Qian Liu

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Xiao ZhangMax Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada.
Sanoji WijenayakeDepartment of Biology, University of Winnipeg, Winnipeg, MB, Canada.
Shakhawat HossainDepartment of Mathematics and Statistics, University of Winnipeg, Winnipeg, MB, Canada.
Qian LiuMax Rady College of Medicine, University of Manitoba, Winnipeg, MB, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Alzheimer's Disease (AD) is heterogeneous and shows complex interconnected pathways at various biological levels. Risk scores contribute greatly to disease prognosis and biomarker discovery but typically represent generic risk factors. However, large-scale multi-omics data can generate individualized risk factors. Filtering these risk factors with brain-derived extracellular vesicles (EVs) could yield key pathologic pathways and vesicular vehicles for treatment delivery. Methods: A list of 460 EV-related genes was curated from brain tissue samples in the ExoCarta database. This list was used to select genes from transcriptomics, proteomics, and DNA methylation data. Significant risk factors included demographic features (age, sex) and genes significant for progression in transcriptomics data. These genes were selected using Cox regression, aided by the Least Absolute Shrinkage and Selection Operator (LASSO), and were used to construct three risk models at different omics levels. Gene signatures from the significant risk factors were used as biomarkers for further evaluation, including gene set enrichment analysis (GSEA) and drug perturbation analysis. Results: Nine EV-related genes were identified as significant risk factors. All three risk models predicted high/low risk groups with significant separation in Kaplan-Meier analysis. Training the transcriptomics risk models on EV-related genes yielded better AD classification results than using all genes in an independent dataset. GSEA revealed Mitophagy and several other significant pathways related to AD. Four drugs showed therapeutic potential to target the identified risk factors based on Connectivity Map analysis. Conclusion: The proposed risk score model demonstrates a novel approach to AD using EV-related large-scale multi-omics data. Potential biomarkers and pathways related to AD were identified for further investigation. Drug candidates were identified for further evaluation in biological experiments, potentially transported to targeted tissues via bioengineered EVs.

Indexed as

Alzheimer’s diseasebiomarkersCox regressionextracellular vesicles (EV)LASSOmultiomics

Identifiers

PMID40778305
PMCPMC12328399

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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.