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Gene Set Index Based on Different Modules May Help Differentiate the Mechanisms of Alzheimer’s Disease and Vascular Dementia

Authors Zhou F, Chen D, Chen G, Liao P, Li R, Nong Q, Meng Y, Zou D, Li X

Received 16 December 2020

Accepted for publication 25 February 2021

Published 11 March 2021 Volume 2021:16 Pages 451—463

DOI https://doi.org/10.2147/CIA.S297483

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Zhi-Ying Wu


Fengkun Zhou,1,2,* Deyao Chen,1,2,* Guoying Chen,1,2,* Peiling Liao,1,2 Rongjie Li,1,2 Qingfang Nong,1,2 Youshi Meng,1,2 Donghua Zou,1 Xianfeng Li1,2

1Department of Neurology, The Fifth Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530022, People’s Republic of China; 2Department of Neurology, The First People’s Hospital of Nanning, Nanning, Guangxi, 530022, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Donghua Zou; Xianfeng Li
The Fifth Affiliated Hospital of Guangxi Medical University, 89 Qixing Road, Nanning, Guangxi, 530022, People’s Republic of China
Tel +867712636189
Email [email protected]; [email protected]

Purpose: Alzheimer’s disease (AD) and vascular dementia shared similar symptoms, the aim of the present study was to identify potential differences in the mechanisms underlying the two diseases.
Materials and Methods: The data set including AD, vascular dementia, and control samples was carried out gene differential expression analysis, weighted gene co-expression network analysis, functional enrichment, protein–protein interaction network construction, and least absolute shrinkage and selection operator analysis to reveal the differences in the mechanisms underlying the two diseases and potential diagnostic gene signature.
Results: We identified the gene modules related to AD or vascular dementia. Enrichment analysis of module genes and construction of a protein–protein interaction network suggested that the “brown” module may be involved in a chemokine pathway, the “blue” module may be involved in cortisol synthesis and secretion, and the “turquoise” module may be involved in cholinergic synapse transmission. The hub gene-based signature index may be a biomarker of AD and vascular dementia and may even differentiate the two diseases from each other with high area under curve.
Conclusion: Our results identified not only core pathways involved in both AD and vascular disease, but also their potentially specific pathways. We proposed the hub gene-based signature index may be useful for diagnosing AD and vascular dementia.

Keywords: Alzheimer’s disease, vascular dementia, weighted gene co-expression network analysis, LASSO, WGCNA

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