Oxidative Stress-Related Mechanisms in Schizophrenia Pathogenesis and New Treatment Perspectives

Figure 1

Oxidative stress-related mechanisms of schizophrenia pathogenesis. The involvement of each mechanism increases the likelihood of phenotypic realization and the manifestation of schizophrenia. The red line indicates the probability of developing schizophrenia; various causal mechanisms are plotted along the axes. All of these mechanisms can be involved both together and separately and during different critical periods. Various genetic causes (1) contribute to the increased susceptibility of individuals to oxidative stress. Genetic predisposition due to environmental impact at various critical periods contributes to redox imbalance, which leads to dysregulation of gene expression and redox signaling (2). These changes promote mitochondrial dysfunction and metabolic abnormalities (3). These processes, in turn, contribute to aberrant neuronal development (4) and abnormal myelination (5). These factors promote the neurotransmitter anomalies (6) and dysfunction of parvalbumin-positive interneurons (7). Immune dysfunction (8) also contributes to oxidative imbalance. All these mechanisms ultimately contribute to the manifestation of psychosis and the development of schizophrenia. Abbreviations: PV = parvalbumin; NMDAR = N-methyl-D-aspartate receptor.