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Depressive disorder results in significant functional impairment. Cognitive deficits are one of the causes of this disruption. There is a lower degree of impaired cognition in depression than in dementia or psychotic disorders; however, it is not just a state marker, but also trait marker. Cognitive dysfunctions in major depression can be observed not just as consequence of depressive symptoms during acute episode, but also in remitted patients. Impaired cognitive functioning has been found even in first-episode patients. Patients with depression have impairments of both "cold cognition" (emotion-independent: executive functions, attention, working memory, general and psychomotor processing speed) and "hot cognition" (emotionladen: social misinterpretation, negative bias). Cognitive deficits are often residual symptoms, significantly interfere with everyday functioning, contribute to functional impairments. Patients themselves subjectively perceive low cognitive performance; the primary instruments for objective detection and assessment are neuropsychological tests. In clinical practice, these tests are not usually available, simple self-reported measures can be used instead. Both non-pharmacological (e.g., cognitive remediation) and pharmacological interventions are used for treatment of cognitive deficits in depression. Preliminary data indicate that a combination of remediation and pharmacotherapy can be more efficacious than drugs alone. So far, there is a limited number of randomized trials with antidepressants, either placebo-controlled or head-to-head comparisons, primarily testing procognitive effects in non-geriatric depressed patients. As for drug therapy, there is evidence that dual (duloxetine) and multimodal (vortioxetine) antidepressants are effective. Other agents (e.g., stimulants, cognitive drugs, hormones, glutamatergic antagonists, nutritional supplements) are being experimentally tested as adjuvant therapy. [ABSTRACT FROM AUTHOR]

Serotonergic agonist psilocybin is a psychedelic with antidepressant potential. Sleep may interact with psilocybin's antidepressant properties like other antidepressant drugs via induction of neuroplasticity. The main aim of the study was to evaluate the effect of psilocybin on sleep architecture on the night after psilocybin administration. Regarding the potential antidepressant properties, we hypothesized that psilocybin, similar to other classical antidepressants, would reduce rapid eye movement (REM) sleep and prolong REM sleep latency. Moreover, we also hypothesized that psilocybin would promote slow-wave activity (SWA) expression in the first sleep cycle, a marker of sleep-related neuroplasticity. Twenty healthy volunteers (10 women, age 28–53) underwent two drug administration sessions, psilocybin or placebo, in a randomized, double-blinded design. Changes in sleep macrostructure, SWA during the first sleep cycle, whole night EEG spectral power across frequencies in non-rapid eye movement (NREM) and REM sleep, and changes in subjective sleep measures were analyzed. The results revealed prolonged REM sleep latency after psilocybin administration and a trend toward a decrease in overall REM sleep duration. No changes in NREM sleep were observed. Psilocybin did not affect EEG power spectra in NREM or REM sleep when examined across the whole night. However, psilocybin suppressed SWA in the first sleep cycle. No evidence was found for sleep-related neuroplasticity, however, a different dosage, timing, effect on homeostatic regulation of sleep, or other mechanisms related to antidepressant effects may play a role. Overall, this study suggests that potential antidepressant properties of psilocybin might be related to changes in sleep. [ABSTRACT FROM AUTHOR]