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Research Paper|Volume 12, Issue 21|pp 21798—21808

Molecular identification of protein kinase C beta in Alzheimer's disease

Zhike Zhou1, Fenqin Chen1, Shanshan Zhong2, Yi Zhou3, Rongwei Zhang1, Kexin Kang1, Xiaoqian Zhang2, Ying Xu3,4, Mei Zhao5, Chuansheng Zhao2
  • 1Department of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China
  • 2Department of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China
  • 3Computational Systems Biology Lab, Department of Biochemistry and Molecular Biology and Institute of Bioinformatics, The University of Georgia, Athens, GA 30602, USA
  • 4Cancer Systems Biology Center, The China-Japan Union Hospital, Jilin University, Changchun, PR China
  • 5Department of Cardiology, The Shengjing Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China
* Equal contribution
Received: June 29, 2020Accepted: August 15, 2020Published: November 7, 2020
https://doi.org/10.18632/aging.103994

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.

Abstract

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.