Fig. 1: General scheme of hypothesis-driven gene selection in different pathways and the corresponding boxplots of selected gene expression.

A Genes selected based on the hypothesis that redox dysregulation, neuroinflammation and NMDAR hypofunction act in a feedforward loop of processes to converge on oxidative stress, which affects parvalbumin expressing interneurons during their maturation as a core pathophysiological mechanism in SZ. Genes that were shown to be altered in SZ, were selected in 10 different pathways, namely the antioxidant pathway, the GSH related pathway, inflammation, the complement, the collagen synthesis/degradation, MMPs, RAGE, arginine metabolism, BDNF and GABAergic maturation. The protein name is represented in this scheme and corresponding gene name is established in Supplementary Fig. 1. B Boxplot of selected genes, after a two-way-ANOVA analysis with 3 factors, the treatment (T: tBHQ and DMSO), the status (Gr: patient or control) and the genotype (G: GAG-gclc HR and LR). Genes from different pathways were found to be significantly different between patients and controls, and the GAG-gclc polymorphism was found to modulate the different responses in patients and in controls, which highlight the important role of the genetic background for redox vulnerability. C GCL activity was significantly decreased in the HR genotype patients and controls, highlighting the functional consequence of the GAG-gclc polymorphism. Data are expressed as mean ± s.e.d. (N = 15) *P < 0.05; **P < 0.01; ***P < 0.001.