Abstract
Schizophrenia is considered a neurodevelopmental and neurodegenerative disorder, which is based on morphological abnormalities in the brain. Cognitive impairment is a core symptom of the illness, and has been suggested a major predictor of functional outcomes. Reduction of parvalbumin (PV)-positive γ- aminobutyric acid (GABA) interneurons has been associated with the pathophysiology of schizophrenia, in view of the link between the abnormality of GABA neurons and cognitive impairments of the disease. It is assumed that decreased glutamatergic projections and PV-positive GABA interneurons in the prefrontal cortex result in sustained neural firing and gamma oscillation, leading to impaired cognitive function. Therefore, it is important to develop novel pharmacotherapy targeting morphological abnormalities, especially, GABA neurons and their activities. -817MA, a novel neurotrophic agent, ameliorates loss of PV- positive GABA neurons in the medial prefrontal cortex and reduction of gamma- band activity, as well as cognitive dysfunction in animal model of schizophrenia. In conclusion, drugs with anti-oxidant effects, such as T-817MA, are likely to prevent the onset and/or progression of schizophrenia.
