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

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.