Abstract
Cognitive deficit is considered as the core impairment in schizophrenia, it correlates with outcomes more than psychotic symptoms. Cognitive dysfunction can be found in the prodromal phases, in first episodes and in chonic phases of the illness.
Therapeutic options are limited, nonpharmacological interventions (cognitive remediation, neurostimulation) or drugs that modulate dopaminergic, glutamatergic, serotoninergic, cholinergic, or GABA neurotransmitter system can be used. In clinical practice, the most available procognitive drugs are antipsychotics; however, their clinical effect is small.
New serotonin-dopamine antagonist lurasidone has a unique receptor profile that suggests positive effect on cognition: 5-HT7 and α2C receptor antagonism, 5-HT1A agonism, low affinity to D4 receptors. Lurasidone in animal studies reliably improved experimentally impaired memory and learning functions and enhanced neural plasticity.
Clinical data on the procognitive efficacy of lurasidone are based on a short-term comparison with ziprasidone and mainly on a double-blind study with quetipine XR. Lurasidone was superior to the comparators in cognitive performance of schizophrenia patients in both short- and long-term treatment.
Reduction of cognitive deficit was associated with improvement of patients' functional capacity.