Abstract
Aim: The purpose of this study was to elucidate the potential mechanisms of Alzheimer’s disease (AD) induced by Type 2 diabetes mellitus (T2DM) through bioinformatics analysis, to provide new treatment targets for this disease. Methods: We used weighted gene coexpression network analysis and differentially expressed genes analysis to identify significantly differentially expressed genes shared by T2DM and AD. Molecular docking was used to predict possible protein targets for T2DM-induced AD. Results: The direct interaction of CD44 and STAT3 may play a significant role in the development of T2DM-induced AD. Conclusion: A new approach to treating T2DM-associated AD may be provided by these hub genes and their predicted molecular targets.
Supplementary data
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Acknowledgments
The authors are grateful to all the staff in the Public Experimental Research Center and Experimental Animal Center of Xuzhou Medical University for their support and help during the experiments.
Financial & competing interests disclosure
This work was supported by grants from the National Natural Science Foundation of China (82271205), the Xuzhou Special Fund for promoting scientific and technological innovation (KC21062) and the Jiangsu Province graduate student innovation project (KYCX22-2889). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Ethical conduct of research
Animal experimental procedures were carried out in accordance with the guidelines described in the 2011 revised Regulations on the Administration of Laboratory Animal Affairs in China and approved by the Institutional Animal Care and Use Committee of Xuzhou Medical University. All data that support the findings of this study are included in this article and are available from the corresponding author upon reasonable request.