Research Paper Volume 12, Issue 21 pp 21798—21808
Molecular identification of protein kinase C beta in Alzheimer's disease
- 1 Department of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China
- 2 Department of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China
- 3 Computational Systems Biology Lab, Department of Biochemistry and Molecular Biology and Institute of Bioinformatics, The University of Georgia, Athens, GA 30602, USA
- 4 Cancer Systems Biology Center, The China-Japan Union Hospital, Jilin University, Changchun, PR China
- 5 Department of Cardiology, The Shengjing Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China
Received: June 29, 2020 Accepted: August 15, 2020 Published: November 7, 2020https://doi.org/10.18632/aging.103994
How to Cite
Copyright: © 2020 Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The purpose of this study was to investigate the potential roles of protein kinase C beta (PRKCB) in the pathogenesis of Alzheimer’s disease (AD). We identified 2,254 differentially expressed genes from 19,245 background genes in AD versus control as well as PRKCB-low versus high group. Five co-expression modules were constructed by weight gene correlation network analysis. Among them, the 1,222 genes of the turquoise module had the strongest relation to AD and those with low PRKCB expression, which were enriched in apoptosis, axon guidance, gap junction, Fc gamma receptor (FcγR)-mediated phagocytosis, mitogen-activated protein kinase (MAPK) and vascular endothelial growth factor (VEGF) signaling pathways. The intersection pathways of PRKCB in AD were determined, including gap junction, FcγR-mediated phagocytosis, MAPK and VEGF signaling pathways. Based on the performance evaluation of the area under the curve of 75.3%, PRKCB could accurately predict the onset of AD. Therefore, low expressions of PRKCB was a potential causative factor of AD, which might be involved in gap junction, FcγR-mediated phagocytosis, MAPK and VEGF signaling pathways.