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2000;71(2):643S-649S

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Then we turn to a discussion of clinical and pre-clinical findings of redox impairment that induce brain pathology in schizophrenia, through mechanisms that likely involve aberrant inflammatory responses, mitochondrial dysfunction, oligodendrocyte abnormalities, epigenetic changes, hypoactive N -methyl-D-aspartate (NMDA) glutamate receptors and the impairment of fast-spiking gamma-aminobutyric acid (GABA) interneurons ( see Figure 1)