Potential Roles of Redox Dysregulation in the Development of Schizophrenia

Converging evidence implicates redox dysregulation as a pathological mechanism driving the emergence of psychosis. Increased oxidative damage and decreased capacity of intracellular redox modulatory systems are consistent findings in persons with schizophrenia as well as in persons at clinical high-risk who subsequently developed frank psychosis. Levels of glutathione, a key regulator of cellular redox status, are reduced in the medial prefrontal cortex, striatum and thalamus in schizophrenia. In humans with schizophrenia and in rodent models recapitulating various features of schizophrenia, redox dysregulation is linked to reductions of parvalbumin containing GABA interneurons and volumes of their perineuronal nets, white matter abnormalities and microglia activation.
Source: Biological Psychiatry - Category: Psychiatry Authors: Tags: Review Source Type: research