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Peer-reviewedCC BY 4.0Biomolecules

Integrated Multi-Omics Analysis Reveals ACO2 as an Oxidative-Stress-Related Biomarker in Alzheimer’s Disease

  • Wenbo Dou1,2,3
  • Xue Chen1
  • Hang Hong1
  • Qiong Liu1
  • Sa Xiao1
  • Lian Li1
  • Jiancheng Yu2,3
  • Chunlan Tang1,3
  1. 1School of Public Health, Health Science Center, Institute of One Health Science, Ningbo University, Ningbo 315211, China
  2. 2Faculty of Electrical Engineering and Computer Science, Ningbo University, Ningbo 315211, China
  3. 3Zhejiang Engineering Research Center of Advanced Mass Spectrometry and Clinical Application, Institute of Mass Spectrometry, Ningbo University, Ningbo 315211, China
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Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory impairment. Oxidative stress plays an important role in disease progression in AD. However, the molecular mechanisms underlying oxidative stress in AD remain unclear and reliable biomarkers for its detection have not been identified. In this study, bioinformatics analyses integrating differential expression analysis and weighted gene co-expression network analysis were performed to identify oxidative-stress-related differentially expressed genes. Using machine learning algorithms, ACO2 was identified as a significantly downregulated hub gene associated with AD. Single-cell transcriptomic analysis further showed markedly reduced ACO2 expression levels in hippocampal neurons of patients with AD. To validate these findings, proteomic analysis, quantitative real-time polymerase chain reaction (qPCR), and Western blotting were performed in a mouse model of AD. These results confirmed decreased ACO2 mRNA and protein expression levels in the hippocampus. Consistently, qPCR analysis of peripheral blood samples from patients with AD revealed significantly reduced ACO2 expression levels compared to those in healthy controls. Collectively, these findings identified ACO2 as an oxidative-stress-related biomarker associated with AD and suggested its potential value as an AD-related candidate biomarker.

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Cite

BibTeXRIS
BibTeX
@article{dou2026integrated,
  title = {{Integrated Multi-Omics Analysis Reveals ACO2 as an Oxidative-Stress-Related Biomarker in Alzheimer’s Disease}},
  author = {Wenbo Dou and Xue Chen and Hang Hong and Qiong Liu and Sa Xiao and Lian Li and Jiancheng Yu and Chunlan Tang},
  journal = {Biomolecules},
  year = {2026},
  month = oct,
  doi = {10.3390/biom16101435},
  url = {https://www.mdpi.com/2218-273X/16/10/1435},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Integrated Multi-Omics Analysis Reveals ACO2 as an Oxidative-Stress-Related Biomarker in Alzheimer’s Disease
AU  - Wenbo Dou
AU  - Xue Chen
AU  - Hang Hong
AU  - Qiong Liu
AU  - Sa Xiao
AU  - Lian Li
AU  - Jiancheng Yu
AU  - Chunlan Tang
PY  - 2026
DA  - 2026/10/01
JO  - Biomolecules
DO  - 10.3390/biom16101435
UR  - https://www.mdpi.com/2218-273X/16/10/1435
AB  - Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory impairment. Oxidative stress plays an important role in disease progression in AD. However, the molecular mechanisms underlying oxidative stress in AD remain unclear and reliable biomarkers for its detection have not been identified. In this study, bioinformatics analyses integrating differential expression analysis and weighted gene co-expression network analysis were performed to identify oxidative-stress-related differentially expressed genes. Using machine learning algorithms, ACO2 was identified as a significantly downregulated hub gene associated with AD. Single-cell transcriptomic analysis further showed markedly reduced ACO2 expression levels in hippocampal neurons of patients with AD. To validate these findings, proteomic analysis, quantitative real-time polymerase chain reaction (qPCR), and Western blotting were performed in a mouse model of AD. These results confirmed decreased ACO2 mRNA and protein expression levels in the hippocampus. Consistently, qPCR analysis of peripheral blood samples from patients with AD revealed significantly reduced ACO2 expression levels compared to those in healthy controls. Collectively, these findings identified ACO2 as an oxidative-stress-related biomarker associated with AD and suggested its potential value as an AD-related candidate biomarker.
SN  - 2218-273X
ER  -