***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND Previous studies have demonstrated an enhancement of hippocampal-dependent declarative memory consolidation , associated slow wave sleep ( SWS ) and slow wave activity ( SWA ) after weak slow oscillatory stimulation ( so-tDCS ) during early non-rapid eye movement sleep ( NREM ) in young adults . Recent studies in older individuals could not confirm these findings . However , it remained unclear if this difference was due to variations in study protocol or to the age group under study . OBJECTIVE /HYPOTHESIS Here , we asked if so-tDCS promotes neurophysiological events and associated sleep-dependent memory in the visuo-spatial domain in older adults , using a stimulation protocol that closely resembled the one employed in young adults . METHODS In a r and omized , placebo-controlled single-blind ( participant ) crossover study so-tDCS ( 0.75 Hz ; max . current density 0.522 mA/cm(2 ) ) vs. sham stimulation was applied over the frontal cortex of 21 healthy older subjects . Impact of stimulation on frequency b and activity ( linear mixed models ) , two declarative and one procedural memory tasks ( repeated measures ANOVA ) and percentage of sleep stages ( comparison of means ) was assessed . RESULTS so-tDCS , as compared to sham , increased SWA and spindle activity immediately following stimulation , accompanied by significantly impaired visuo-spatial memory consolidation . Furthermore , verbal and procedural memory remained unchanged , while percentage of NREM sleep stage 4 was decreased over the entire night ( uncorrected ) . CONCLUSION so-tDCS  increased SWA and spindle activity in older adults , events previously associated with stimulation-induced improved consolidation of declarative memories in young subjects . However , consolidation of visuo-spatial ( primary outcome ) and verbal memories was not beneficially modulated , possibly due to decline in SWS over the entire night that may have prevented and even reversed immediate beneficial effects of so-tDCS on SWA Background Disturbance in sleep quality is a symptom of Major Depressive Disorder ( MDD ) and Bipolar Disorder ( BD ) and thus improving quality of sleep is an important aspect of successful treatment . Here , a prospect i ve , double-blind , r and omized , placebo-controlled study examined the effect of olanzapine ( an atypical antipsychotic ) augmentation therapy on sleep architecture , specifically slow wave sleep ( SWS ) , in the treatment of depression . The effect of olanzapine augmentation therapy on other features of sleep ( e.g. , sleep continuity ) and depression ( e.g. , illness severity and cognitive function ) were also determined . Methods Patients currently experiencing a major depressive episode and who were on a stable medication were included . Sleep architecture was measured by overnight ambulatory polysomnography . Illness severity was determined using the Montgomery-Asberg Depression Rating Scale ( MADRS ) . Cognitive function was examined using Cambridge Neuropsychological Test Automated Battery ( CANTAB ) : Spatial Working Memory ( SWM ) , Spatial Span ( SSP ) , and Reaction Time ( RTI ) tasks . Polysomnographs , clinical measures and cognitive tests were administered at baseline , after 2–4 days of treatment and after 28–31 days of treatment . Twenty-five patients participated in the study ( N = 10 , N = 15 for placebo and olanzapine treated groups respectively ) . Results The primary objective of the study was to assess the objective ( polysomnographic ) changes in sleep quality , defined as changes in SWS , following olanzapine treatment for depression . Latency to but not duration of SWS was found to significantly differ between olanzapine- and placebo-treated participants ( Hedge ’s g : 0.97 , 0.13 respectively ) . A significant improvement in olanzapine-treated participants over placebo-treated participants was observed in secondary outcome measures , including sleep efficiency , total sleep time , and sleep latency . Secondary objectives assessed the subjective changes in sleep quality parameters and correlated them with measures of illness severity and changes in cognition . MADRS scores were significantly improved in olanzapine-treated participants over time but not more than placebo treatment . There was no significant difference between olanzapine- and placebo-treated participants in SWM , SSP or RTI tasks . Conclusions Olanzapine augmentation treatment generally did not improve SWS but did improve sleep continuity and depression .  Olanzapine may be one of few medications that improve sleep continuity , thus directly targeting symptoms of depression . Trial registration Clinical Trials.gov , NCT00520507 Five patients with nocturnal myoclonus ( periodic leg movements during sleep ) , mean age 59.6 years , were monitored lygraphically for fifteen successive nights . Using a double‐blind drug study design with placebo at baseline , we inestigated the effect of baclofen on these patients . All patients had the repetitive sleep‐related abnormal movements dring both the baseline nights and those on which baclofen had been administered . The number of movements varied during the four baseline nights , but the movements induced sleep fragmentation , i.e. , very short electroencepha graphic changes . Baclofen increased the number of movements but decreased their amplitude during non – rapid eye movevement ( REM ) sleep and shortened the interval between movements . Its effect on sleep was dose related : as dosages Ceased , delta sleep progressively increased and REM sleep decreased . Sleep fragmentation result ing from muscle aches decreased , as indicated by the diminution in alpha electroencephalographic arousals and K complexes . Baclo‐dosages of 20 mg and 40 mg were the most efficacious Acoustic stimulation methods applied during sleep in young adults can increase slow wave activity ( SWA ) and improve sleep-dependent memory retention . It is unknown whether this approach enhances SWA and memory in older adults , who generally have reduced SWA compared to younger adults . Additionally , older adults are at risk for age-related cognitive impairment and therefore may benefit from non-invasive interventions . The aim of this study was to determine if acoustic stimulation can increase SWA and improve declarative memory in healthy older adults . Thirteen participants 60–84 years old completed one night of acoustic stimulation  and one night of sham stimulation in r and om order . During sleep , a real-time algorithm using an adaptive phase-locked loop modeled the phase of endogenous slow waves in midline frontopolar electroencephalographic recordings . Pulses of pink noise were delivered when the upstate of the slow wave was predicted . Each interval of five pulses ( “ ON interval ” ) was followed by a pause of approximately equal length ( “ OFF interval ” ) . SWA during the entire sleep period was similar between stimulation and sham conditions , whereas SWA and spindle activity were increased during ON intervals compared to matched periods during the sham night . The increases in SWA and spindle activity were sustained across almost the entire five-pulse ON interval compared to matched sham periods . Verbal paired-associate memory was tested before and after sleep . Overnight improvement in word recall was significantly greater with acoustic stimulation compared to sham and was correlated with changes in SWA between ON and OFF intervals . Using the phase-locked-loop method to precisely target acoustic stimulation to the upstate of sleep slow oscillations , we were able to enhance SWA and improve sleep-dependent memory storage in older adults , which strengthens the theoretical link between sleep and age-related memory integrity STUDY OBJECTIVES Sodium oxybate ( SO ) is a GABAβ agonist used to treat the sleep disorder narcolepsy . SO was shown to increase slow wave sleep ( SWS ) and EEG delta power ( 0.75 - 4.5 Hz ) , both indexes of NREM sleep ( NREMS ) intensity and depth , suggesting that SO enhances recuperative function of NREM . We investigated whether SO induces physiological deep sleep . DESIGN SO was administered before an afternoon nap or before the subsequent experimental night in 13 healthy volunteers . The effects of SO were compared to baclofen ( BAC ) , another GABAβ receptor agonist , to assess the role of GABAβ receptors in the SO response . MEASUREMENTS AND RESULTS As expected , a nap significantly decreased sleep need and intensity the subsequent night . Both drugs reversed this nap effect on the subsequent night by decreasing sleep latency and increasing total sleep time , SWS during the first NREMS episode , and EEG delta and theta ( 0.75 - 7.25 Hz ) power during NREMS . The SO-induced increase in EEG delta and theta power was , however , not specific to NREMS and was also observed during REM sleep ( REMS ) and wakefulness . Moreover , the high levels of delta power during a nap following SO administration did not affect delta power the following night . SO and BAC taken before the nap did not improve subsequent psychomotor performance and subjective alertness , or memory consolidation . Finally , SO and BAC strongly promoted the appearance of sleep onset REM periods . CONCLUSIONS The SO-induced EEG slow waves seem not to be functionally similar to physiological slow waves . Our findings also suggest a role for GABAβ receptors in REMS generation In humans , weak transcranial direct current stimulation ( tDCS ) modulates excitability in the motor , visual , and prefrontal cortex . Periods rich in slow-wave sleep ( SWS ) not only facilitate the consolidation of declarative memories , but in humans , SWS is also accompanied by a pronounced endogenous transcortical DC potential shift of negative polarity over frontocortical areas . To experimentally induce widespread extracellular negative DC potentials , we applied anodal tDCS ( 0.26 mA/cm2 ) repeatedly ( over 30 min ) bilaterally at frontocortical electrode sites during a retention period rich in SWS . Retention of declarative memories ( word pairs ) and also nondeclarative memories ( mirror tracing skills ) learned previously was tested after this period and compared with retention performance after placebo stimulation as well as after retention intervals of wakefulness . Compared with placebo stimulation , anodal tDCS during SWS-rich sleep distinctly increased the retention of word pairs ( p < 0.005 ) . When applied during the wake retention interval , tDCS did not affect declarative memory . Procedural memory was also not affected by tDCS .  Mood was improved both after tDCS during sleep and during wake intervals . tDCS  increased sleep depth toward the end of the stimulation period , whereas the average power in the faster frequency b and s ( θ , α , and β ) was reduced . Acutely , anodal tDCS increased slow oscillatory activity <3 Hz . We conclude that effects of tDCS involve enhanced generation of slow oscillatory EEG activity considered to facilitate processes of neuronal plasticity . Shifts in extracellular ionic concentration in frontocortical tissue ( expressed as negative DC potentials during SWS ) may facilitate sleep-dependent consolidation of declarative memories BACKGROUND Slow oscillations ( < 1 Hz ) during slow wave sleep ( SWS ) promote the consolidation of declarative memory .  Children with attention-deficit/hyperactivity disorder ( ADHD ) have been shown to display deficits in sleep-dependent consolidation of declarative memory supposedly due to dysfunctional slow brain rhythms during SWS . OBJECTIVE Using transcranial oscillating direct current stimulation ( toDCS ) at 0.75 Hz , we investigated whether an externally triggered increase in slow oscillations during early SWS elevates memory performance in children with ADHD . METHODS 12 children with ADHD underwent a toDCS and a sham condition in a double-blind crossover study design conducted in a sleep laboratory . Memory was tested using a 2D object-location task . In addition , 12 healthy children performed the same memory task in their home environment . RESULTS Stimulation enhanced slow oscillation power in children with ADHD and boosted memory performance to the same level as in healthy children . CONCLUSION These data indicate that increasing slow oscillation power during sleep by toDCS can alleviate declarative memory deficits in children with ADHD Interleukin-6 ( IL-6 ) is a proinflammatory cytokine that has been shown to mediate , in addition to immune reactions , various endocrine and central nervous components of the acute phase response . In this context , the present study aim ed to specify the contributions of IL-6 to the regulation of pituitary-adrenal secretory activity and GH and TSH secretion , as well as to the regulation of central nervous sleep and mood in healthy men . Effects of a low dose of IL-6 ( 0.5 microgram/kg body weight ) were assessed , inducing plasma IL-6 concentrations closely comparable with those typically observed after infectious challenge . Each of the 16 male subjects participated in two 14-h sessions ( between 1800 and 0800 h ) , receiving either placebo or human recombinant IL-6 sc at 1900 h. Blood was collected repeatedly to determine plasma hormone levels , serum concentrations of cytokines , and C-reactive protein . Moreover , mood was assessed , and sleep recordings were obtained between 2300 and 0700 h. The cytokine induced a prolonged increased in plasma concentrations of ACTH and cortisol ( P < 0.001 ) , but led to a decrease in TSH concentrations ( P < 0.01 ) . In response to IL-6 , subjects reported fatigue and felt more inactive and less capable of concentrating than after placebo . Sleep architecture was altered significantly by the cytokine . Slow-wave sleep was decreased during the first half and increased during the second half of sleep . Rapid eye movement sleep during the entire nocturnal sleep time was significantly decreased . After IL-6 , body temperature rose slightly . C-reactive protein concentrations were dramatically increased 12.5 h after substance administration ( P < 0.001 ) . IL-6 did not affect serum concentrations of IL-2 , IL-8 , interferon-alpha , and interferon-gamma . The results underscore the importance of IL-6 in the cascade of cytokines for the neuroendocrine response during the acute 
    Output:
    
Closed-loop , in-phase auditory stimulation enhanced verbal declarative memory in healthy adults .
Electrical stimulation using so-tDCS showed some efficacy in promoting verbal declarative memory , picture recognition memory , and location memory .
Interleukin-6 and sodium oxybate enhanced declarative verbal memory , while tiagabine and sodium oxybate improved some non-memory measures of cognitive performance .