"Pharmacological management of cognitive deficit in schizophrenia" . "1"^^ . "[6131C84BAE89]" . "1"^^ . "978-1-60741-957-0" . "Psychology Research Progress" . . . . "96002" . "P(1M0517)" . "Pharmacological management of cognitive deficit in schizophrenia"@en . "Cognitive Deficit in Mental and Neurological Disorders" . "13"^^ . "RIV/00023752:_____/13:43914450" . . . "glutamate; norepinephrine; dopamine; antipsychotics; cognition; schizophrenia"@en . "454"^^ . "Pharmacological management of cognitive deficit in schizophrenia" . . "https://www.novapublishers.com/catalog/product_info.php?products_id=10607" . . . . . . . . . . "Cognitive deficit represents the core impairment in schizophrenia that fundamentally affects course and functional outcome of illness. Thus far, generally held views claim that conventional antipsychotics are less effective in cognitive remediation; furthermore, cognition may be worsened by the adjuvant anticholinergic medication used to alleviate from side effects. However, several earlier and recent reports indicated that a low dosage of typical antipsychotics may possess procognitive properties. Unequivocally positive effects of virtually all second-generation antipsychotics in remediation of a cognitive deficit have been shown in both individual studies and meta-analyses. The key role in cognition is played by dopamine activity in the prefrontal cortex. Dopamine action is mediated through D1 receptors, as evidenced by the improvement of cognitive performance following administration of D1 agonists. Stimulation of dopamine neurotransmission is rate-limited: low doses enhance cognition whereas higher doses may cause cognitive impairments. Dopamine activity can be also modulated indirectly, via serotonin receptor system, either with 5-HT1a agonists or 5-HT2 antagonists."@en . . . "Pharmacological management of cognitive deficit in schizophrenia"@en . "RIV/00023752:_____/13:43914450!RIV14-MSM-00023752" . . "Cognitive deficit represents the core impairment in schizophrenia that fundamentally affects course and functional outcome of illness. Thus far, generally held views claim that conventional antipsychotics are less effective in cognitive remediation; furthermore, cognition may be worsened by the adjuvant anticholinergic medication used to alleviate from side effects. However, several earlier and recent reports indicated that a low dosage of typical antipsychotics may possess procognitive properties. Unequivocally positive effects of virtually all second-generation antipsychotics in remediation of a cognitive deficit have been shown in both individual studies and meta-analyses. The key role in cognition is played by dopamine activity in the prefrontal cortex. Dopamine action is mediated through D1 receptors, as evidenced by the improvement of cognitive performance following administration of D1 agonists. Stimulation of dopamine neurotransmission is rate-limited: low doses enhance cognition whereas higher doses may cause cognitive impairments. Dopamine activity can be also modulated indirectly, via serotonin receptor system, either with 5-HT1a agonists or 5-HT2 antagonists." . "Nova Science Publishers" . "New York" . "Mohr, Pavel" . .