***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 Recent findings suggest that there may be a relationship between excessive daytime sleepiness ( EDS ) and cognitive deficits . This study aims to determine to what extent EDS is predictive of cognitive impairment in an elderly population . METHODS A total of 1026 individuals 60 years or older representative of the general population living in the metropolitan area of Paris , France , were interviewed by telephone using the Sleep-EVAL expert system . To find these individuals , 7010 r and omly selected households were called : 1269 had at least 1 household member in this age range ( participation rate , 80.9 % ) . In addition to Diagnostic and Statistical Manual of Mental Disorders , Fourth Edition , and International Classification of Sleep Disorders diagnoses , the system administered to participants the Psychological General Well-being Schedule , the Cognitive Difficulties Scale ( MacNair-R ) , and an independent living scale . RESULTS Excessive daytime sleepiness was reported by 13.6 % of the sample , with no significant difference among age groups . Compared with nonsleepy participants , those with EDS were at increased risk of cognitive impairment on all the dimensions of the MacNair-R scale after controlling for age , sex , physical activity , occupation , organic diseases , use of sleep or anxiety medication , sleep duration , and psychological well-being . The odd ratios were 2.1 for attention-concentration deficits , 1.7 for praxis , 2.0 for delayed recall , 2.5 for difficulties in orientation for persons , 2.2 for difficulties in temporal orientation , and 1.8 for prospect i ve memory . CONCLUSIONS Among elderly individuals in the general population , EDS is an important risk factor for cognitive impairment . A complaint of EDS by an elderly patient should signal the possibility of an underlying cognitive impairment in need of evaluation To assess age- , sex- , and subtype-specific incidence rates of dementia and to calculate the risk of dementia , the authors performed a large , community-based , prospect i ve cohort study on dementia as part of the Rotterdam Study . Participants were recruited among residents of a suburb of Rotterdam , aged 55 years and older . Baseline examinations took place between 1990 and 1993 . The average follow-up was 2.1 years . Screening for dementia followed a three-stage protocol . Medical records of subjects who had died or could not be examined in person were evaluated . Of 7,046 subjects who were nondemented at baseline , 162 developed dementia during 15,135 person-years of follow-up , result ing in an overall incidence rate of 10.7 per 1,000 person-years . From the youngest to the oldest 5-year age category , the incidence rate increased from 0.6 to 97.2 per 1,000 person-years . Only in men did the increase level off after age 85 . Overall , the incidence rate per 1,000 person-years was 7.7 for Alzheimer 's disease and 1.5 for vascular dementia . Dementia incidence rates and dementia-free Kaplan-Meier survival tables were used to calculate age- and sex-specific cumulative risks of dementia . Although the incidence rates of men and women up to age 85 were similar , the lifetime risk of dementia for 55-year-old women was twice as high as for men ( 0.33 vs. 0.16 ) , reflecting both the higher life expectancy of women and the higher dementia risk at very old age STUDY OBJECTIVES To examine in cognitively intact older men and women the associations between subjective sleep quality and 1-yr incident cognitive impairment . DESIGN Prospect i ve cohort study . SETTING General community . PARTICIPANTS 1,664 cognitively intact individuals age 65 to 96 years . MEASUREMENTS AND RESULTS Sleep quality at baseline was measured using the  Pittsburgh Sleep Quality Index (  PSQI  ) . Cognitive functioning was assessed at baseline and 12 months later using the Mini-Mental State Examination ( MMSE ) . Incident general cognitive impairment was defined according to a follow-up MMSE score below the 15(th ) percentile according to normative data and of at least 2 points below baseline . General cognitive impairments were also separated into amnestic and nonamnestic subtypes according to MMSE delayed recall performance . Associations between sleep quality indicators at baseline and incident cognitive impairment were assessed by odds ratio ( OR ) adjusted for age , education , baseline MMSE score , psychotropic drug use , anxiety , depressive episodes , cardiovascular conditions , and chronic diseases . Results revealed that global PSQI score was significantly linked with incident cognitive impairment ( OR 1.17 , 95 % confidence interval ( CI ) 1.05 - 1.30 ) in men , but not in women . In women , sleep disturbance score ( OR 2.62 , 95 % CI 1.41 - 4.86 ) and long sleep duration ( ≥ 9 hr ; OR 3.70 , 95 % CI 1.49 - 9.17 ) were associated with nonamnestic and amnestic incident cognitive impairment , respectively . In men , short sleep duration ( ≤ 5 hr ; OR 4.95 , 95 % CI 1.72 - 14.27 ) and habitual sleep efficiency score ( OR 1.94 , 95 % CI 1.42 - 2.66 ) were associated with amnestic and general incident cognitive impairment , respectively . CONCLUSIONS Sleep quality in older adults should receive particular attention by clinicians because poor sleep quality can be an early sign of cognitive decline Insomnia is a sleeping disorder , usually studied from a behavioural perspective , with a focus on somatic and cognitive arousal . Recent studies have suggested that an impairment of information processes due to the presence of cortical hyperarousal might interfere with normal sleep onset and /or consolidation . As such , a treatment modality focussing on CNS arousal , and thus influencing information processing , might be of interest . Seventien insomnia patients were r and omly assigned to either a tele-neurofeedback ( n = 9 ) or an electromyography tele-biofeedback ( n = 8) protocol . Twelve healthy controls were used to compare baseline sleep measures . A  polysomnography  was performed pre and post treatment . Total Sleep Time ( TST ) , was considered as our primary outcome variable . Sleep latency decreased pre to post treatment in both groups , but a significant improvement in TST was found only after the neurofeedback ( NFB ) protocol . Furthermore , sleep logs at home showed an overall improvement only in the neurofeedback group , whereas the sleep logs in the lab remained the same pre to post training . Only NFB training result ed in an increase in TST . The mixed results concerning perception of sleep might be related to method ological issues , such as the different locations of the training and sleep measurements OBJECTIVE This article describes an experiment that was design ed to investigate the effects of sleep deprivation on physiological stress responses in healthy adults . METHOD Twenty-six participants , ages 22 - 49 , completed a 3-night laboratory experiment with r and omization to one night of sleep-deprivation or a  normal-sleep control condition . After a night of baseline sleep , 12 participants were sleep deprived and 14 were not . After the sleep manipulation , each participant completed the Trier Social Stress Test , a task that requires delivering a speech and performing difficult arithmetic in front of a stern , three-person panel . The stressor was administered from 5:00 p.m.-5:30 p.m. and saliva sample s were collected 20 and 5 min before ( baseline ) and 5 , 20 , and 40 min after the stressor . Sample s were assayed for cortisol ( a biomarker for the HPA axis ) and alpha-amylase ( a putative biomarker for the sympatho-adrenal medullar system ) . RESULTS Sleep deprivation was associated with higher cortisol levels at baseline ( p < .0001 ) and an amplified cortisol response to the stressor relative to control participants ( pinteraction = 0.0039 ) . Alpha-amylase showed a significant main effect of the stressor ( p = .0026 ) , but there was no effect of sleep loss at baseline or in response to the stressor . CONCLUSIONS Sleep deprivation is associated with both elevated resting cortisol release and with an exaggerated cortisol response to a stressor indicative of elevated HPA axis responses in healthy adults . Individual differences in the magnitude of this response may represent a risk factor for psychological and physical health consequences associated with heightened cortisol exposure OBJECTIVE Sleep disturbances are common in older adults . Little is known about the sleep of cognitively intact older adults and its relationship to subsequent cognitive impairment . The objective of this study was to examine the association between objective sleep-wake measures and risk of incident cognitive impairment . METHODS In this prospect i ve cohort study encompassing four U.S. sites , 1,245 women ( mean age : 82.6 years ) without dementia participated in the Study of Osteoporotic Fractures and completed actigraphy at the baseline visit and comprehensive cognitive assessment at follow-up . The association between sleep-wake patterns measured by actigraphy and risk of incident mild cognitive impairment ( MCI ) and dementia was examined . RESULTS A total of 473 women ( 38 % ) developed cognitive impairment during an average ( SD ) follow-up of 4.9 ( 0.6 ) years ; 290 ( 23.3 % ) developed MCI and 183 ( 14.7 % ) developed dementia . After controlling for multiple potential confounders , women in the lowest quartile of average sleep efficiency ( < 74 % ) had a 1.5-fold higher odds of developing MCI or dementia compared with women in the highest quartile of sleep efficiency ( > 86 % ) ( odds ratio : Q1 versus Q4 1.53 ; 95 % CI : 1.07 , 2.19 ; Wald χ(2 ) [ 1 , N = 1,223 ] = 5.34 for p for trend = 0.03 ) . Longer average sleep latency , but not total sleep time , was also associated with higher odds of developing cognitive impairment . Greater variability in both sleep efficiency and total sleep time was associated with an increased odds of developing MCI or dementia . CONCLUSION Lower average sleep efficiency , longer average sleep latency , and greater variability in sleep efficiency and total sleep time are associated with increased odds of developing cognitive impairment . Further research is needed to explore the mechanisms underlying these associations CONTEXT Sleep-disordered breathing ( characterized by recurrent arousals from sleep and intermittent hypoxemia ) is common among older adults . Cross-sectional studies have linked sleep-disordered breathing to poor cognition ; however , it remains unclear whether sleep-disordered breathing precedes cognitive impairment in older adults . OBJECTIVES To determine the prospect i ve relationship between sleep-disordered breathing and cognitive impairment and to investigate potential mechanisms of this association . DESIGN , SETTING , AND PARTICIPANTS Prospect i ve sleep and cognition study of 298 women without dementia ( mean [ SD ] age : 82.3 [ 3.2 ] years ) who had overnight polysomnography measured between January 2002 and April 2004 in a sub study of the Study of Osteoporotic Fractures . Sleep-disordered breathing was defined as an apnea-hypopnea index of 15 or more events per hour of sleep . Multivariate logistic regression was used to determine the independent association of sleep-disordered breathing with risk of mild cognitive impairment or dementia , adjusting for age , race , body mass index , education level , smoking status , presence of diabetes , presence of hypertension , medication use ( antidepressants , benzodiazepines , or nonbenzodiazepine anxiolytics ) , and baseline cognitive scores . Measures of hypoxia , sleep fragmentation , and sleep duration were investigated as underlying mechanisms for this relationship . MAIN OUTCOME MEASURES Adjudicated cognitive status ( normal , dementia , or mild cognitive impairment ) based on data collected between November 2006 and September 2008 . RESULTS Compared with the 193 women without sleep-disordered breathing , the 105 women ( 35.2 % ) with sleep-disordered breathing were more likely to develop mild cognitive impairment or dementia ( 31.1 % [ n = 60 ] vs 44.8 % [ n = 47 ] ; adjusted odds ratio [ AOR ] , 1.85 ; 95 % confidence interval [ CI ] , 1.11 - 3.08 ) . Elevated oxygen desaturation index ( ≥15 events/hour ) and high percentage of sleep time ( > 7 % ) in apnea or hypopnea ( both measures of disordered breathing ) were associated with risk of developing mild cognitive impairment or dementia ( AOR , 1.71 [ 95 % CI , 1.04 - 2.83 ] and AOR , 2.04 [ 95 % CI , 1.10 - 3.78 ] , respectively ) . Measures of sleep fragmentation ( arousal index and wake after sleep onset ) or sleep duration ( total sleep time ) were not associated with risk of cognitive impairment . CONCLUSION Among older women , those with sleep-disordered breathing compared with those without sleep-disordered breathing had an increased risk of developing cognitive impairment 
    Output:
    
Conclusions The lowest incident risk of cognitive disorders was found at the sleep duration of 7–8 h per day .