Differentially expressed mRNAs of neural signaling pathway genes in peripheral blood leukocytes as biomarkers for schizophrenia

外周血白细胞中神经信号通路基因差异表达的mRNA作为精神分裂症的生物标志物

阅读:2

Abstract

Abnormal neurotransmitter regulation plays a role in the pathogenesis of Schizophrenia (SCZ), and the presence of brain tissue-like aberrant expression in the partial transcriptome of peripheral blood leukocytes from patients with SCZ suggests that these aberrantly expressed genes could be potential diagnostic markers. We designed a case-control study to analyze the association between the expression levels of mRNAs and SCZ in peripheral blood leukocytes and to explore their potential value as diagnostic biomarkers for SCZ. Differentially expressed mRNAs associated with neural signaling pathways were screened by RNA sequencing in a small set, comprising 9 patients with SCZ and 20 controls. A case-control study that included 217 cases and 217 controls was further conducted to verify these mRNAs. The differential expression analysis between cases and controls was performed, followed by restricted cubic spline regression analysis. Gene expression score (GES) was constructed for differentially expressed genes to assess their diagnostic value as biomarkers. In SCZ patients, there were higher expression levels of CREB5, PPP3R1 and PPP1CB (P < 0.05) than in controls. Furthermore, DUSP1 and MAPK13 downregulated in undifferentiated SCZ and acute schizophrenia-like psychotic disorder (P < 0.05), PPP3R1 expression upregulated in paranoid SCZ, undifferentiated SCZ and acute schizophrenia-like psychotic disorder (P < 0.01), and CREB5 exclusively upregulated in paranoid SCZ (P = 0.001), respectively. The risk of SCZ was nonlinearly correlated with DUSP1, GNG10, GNG7, PRKACA, CREB5, PPP3R1 and PPP1CB (P(overall) < 0.05, P(nonlinear) < 0.05). Meanwhile, incorporating these 7 genes into the GES improved the model's area under curve to 0.743, significantly enhancing the diagnostic discriminatory ability for SCZ.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。