PVALB and schizophrenia: Oxidative stress may be involved in the early stage of the pathological course of schizophrenia [10], leading to parvalbumin-positive interneuron dysfunction in the young adult cortex [11]; indeed, the hypofunction of parvalbumin GABAergic interneurons causes an increased glutamate release, which in turn over-stimulates the activation of N-methyl-D-aspartate (NMDA) receptors and subsequent oxidative stress [4,12].