[Mechanisms of neurocognitive deficit development in schizophrenia and current treatment approaches]

This article reviews accumulating knowledge on the signs and pathogenesis of cognitive impairment in schizophrenia. The existing data indicate that cognitive disorders, along with positive and negative symptoms, are key symptoms of schizophrenia. Several neurotransmitter systems, including prefrontal dopaminergic transmission, are involved in the pathological process that causes cognitive disorders. GABAergic and glutamatergic pathophysiological models of schizophrenia are discussed. The main subtype of glutamate receptor NMDA receptor hypofunction is one of the causes of cognitive impairment in schizophrenia. Recent studies revealed alterations in gene expression and activity of kynurenine pathway enzymes in patients with schizophrenia. Concentration of kynurenic acid (KYNA) is increased in the prefrontal cortex of schizophrenca patients and correlated with glutamate, dopamine and acetylcholine levels that reflects the pathophysiological mechanism and degree of cognitive impairment. An overview of animal models of schizophrenia, in particular pharmacological models, is presented. Treatment approaches that promote the recovery of cognitive function are described.