Serum Level of Growth-Associated Protein 43 Is Associated with First-Episode Schizophrenia Patients without Antipsychotic Drugs Treatment.

Nerve growth-associated protein 43 (GAP43) is closely related to neural development, axon regeneration, and synaptic reconstruction and is one of the important markers of neuronal damage. Therefore, in our study, enzyme-linked immunosorbent assay (ELISA) was used to analyze the serum level of GAP43 protein in schizophrenia patients (n = 188), healthy controls (n = 200), and bipolar disorder patients (n = 200). The positive and negative syndrome scale (PANSS) was used to evaluate the mental status of schizophrenia patients, and the Scale of Social Function in Psychosis Inpatients (SSPI) was used to evaluate the social function of schizophrenia patients. According to this study, we found the serum GAP43 level was significantly higher in schizophrenia patients than in bipolar disorder patients, while serum GAP43 levels in bipolar disorder patients were significantly higher than those in control group. When the cut-off value was set as 2.328 ng/mL, the area under the curve (AUC) of serum GAP43 was 0.7795 (95% CI: 0.7431-0.8158) for diagnosis of schizophrenia. The sensitivity and specificity were 92.02% and 65.25%, respectively. However, no correlation between serum GAP43 and the total scores of PANSS scale in schizophrenia patients as well as between serum GAP43 level and SSPI were observed. Therefore, we believe that GAP43 may be a potential diagnostic marker for schizophrenia.

Corrigendum: DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia.

[This corrects the article DOI: 10.3389/fgene.2018.00646.].

DNA methylation and gene expression of the chemokine (C-X-C motif) ligand 1 in patients with deficit and non-deficit schizophrenia.

This study detected the differences in gene expression and DNA methylation of CpG sites in CXCL1 gene and further investigated their associations with clinical symptoms in deficit schizophrenia (DS) and non-deficit schizophrenia (NDS). Pyrosequencing and RT-qPCR were separately used to determine DNA methylation and mRNA expression of CXCL1 gene. Both DNA methylation and expression were significantly different among DS, NDS and healthy control (HC) groups. Correlation analysis revealed that CXCL1 gene expression was associated with the negative syndrome in NDS patients, while no association in DS patients was observed. All together, these results suggest that DS may be a specific subgroup of schizophrenia with the characteristic abnormality of peripheral CXCL1 DNA methylation and gene expression.

DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia.

The biological pathology of deficit schizophrenia (DS) remains unclear. Matrix metalloproteinase 9 (MMP9) might be associated with neural plasticity and glutamate regulation, involved in schizophrenia pathogenesis. This study explores gene expression and DNA methylation of MMP9 in peripheral blood mononuclear cells (PBMCs) and their relationship with clinical symptoms in DS and non-deficit schizophrenia (NDS). Pyrosequencing was used to determine DNA methylation at CpG sites in exon 4 and exon 5 of MMP9 in 51 DS patients, 53 NDS patients and 50 healthy subjects (HC). RT-qPCR was used to detect MMP9 expression. Clinical symptoms were assessed by BPRS, SANS and SAPS scales. MMP9 expression in PBMCs was significantly higher in DS than NDS and HC subjects. Compared to NDS patients, DS patients had significantly lower DNA methylation at individual CpG sites in exon 4 and exon 5 of MMP9. Correlation analysis showed that DNA methylation in exon 4 was negatively correlated with gene expression in DS group. Positive correlation was found between MMP9 expression and negative symptoms in total schizophrenic patients. The social amotivation factor of SANS and negative syndrome of BPRS was negatively correlated with DNA methylation of CpG5-1 in DS patients but not in NDS patients. DS patients showed a specific abnormality of peripheral MMP9 expression and DNA methylation, indicating a pathological mechanism underlying DS as a specific subgroup of schizophrenia.