Adam P. Spira

Sleep-Disordered Breathing, Hypoxia, and Risk of Mild Cognitive Impairment and Dementia in Older Women

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 prospective relationship between sleep-disordered breathing and cognitive impairment and to investigate potential mechanisms of this association. DESIGN, SETTING, AND PARTICIPANTS Prospective 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 substudy 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.

Self-Reported Sleep and β-Amyloid Deposition in Community-Dwelling Older Adults

IMPORTANCE Older adults commonly report disturbed sleep, and recent studies in humans and animals suggest links between sleep and Alzheimer disease biomarkers. Studies are needed that evaluate whether sleep variables are associated with neuroimaging evidence of β-amyloid (Aβ) deposition. OBJECTIVE To determine the association between self-reported sleep variables and Aβ deposition in community-dwelling older adults. DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 70 adults (mean age, 76 [range, 53-91] years) from the neuroimaging substudy of the Baltimore Longitudinal Study of Aging, a normative aging study. EXPOSURE Self-reported sleep variables. MAIN OUTCOMES AND MEASURES β-Amyloid burden, measured by carbon 11-labeled Pittsburgh compound B positron emission tomography distribution volume ratios (DVRs). RESULTS After adjustment for potential confounders, reports of shorter sleep duration were associated with greater Aβ burden, measured by mean cortical DVR (B = 0.08 [95% CI, 0.03-0.14]; P = .005) and precuneus DVR (B = 0.11 [0.03-0.18]; P = .007). Reports of lower sleep quality were associated with greater Aβ burden measured by precuneus DVR (B = 0.08 [0.01-0.15]; P = .03). CONCLUSIONS AND RELEVANCE Among community-dwelling older adults, reports of shorter sleep duration and poorer sleep quality are associated with greater Aβ burden. Additional studies with objective sleep measures are needed to determine whether sleep disturbance causes or accelerates Alzheimer disease.

Sleep‐Disordered Breathing and Cognition in Older Women

OBJECTIVES: To investigate the association between objectively measured sleep‐disordered breathing (SDB) and cognitive impairment in community‐dwelling older women and to determine whether the apolipoprotein E (APOE) ɛ4 allele modifies this association.

Reliability and Validity of the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale in Older Men

BACKGROUND The Pittsburgh Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS) are commonly used to quantify sleep and excessive daytime sleepiness in older adults. These measures, however, have not been comprehensively evaluated for their psychometrics in older men. We determined the internal consistency reliability and construct validity of the PSQI and ESS in a sample of older men. METHODS Participants were 3,059 men (mean age = 76.4 years) in the Osteoporotic Fractures in Men Study (MrOS) who completed the two questionnaires, wrist actigraphy, and a range of additional psychosocial and health measures. RESULTS Internal consistency was adequate for the PSQI (Cronbachs α =.69) and the ESS (α = .70) total scores. PSQI daytime dysfunction and sleep medications components were weakly associated with the total score, but their removal did not notably improve internal consistency. PSQI and ESS totals were associated with each other and with theoretically related variables (ie, actigraphic variables, depressive symptoms, mobility/instrumental activities of daily living, health-related quality of life) in expected directions. The PSQI differentiated participants reporting no sleep disorder from those reporting particular disorders more reliably than the ESS. CONCLUSIONS In general, we found evidence of the internal consistency reliability and construct validity of the PSQI and ESS in older men. Despite low correlation with the PSQI global score, the PSQI daytime dysfunction and sleep medications components do not appreciably reduce the PSQI total scores reliability or validity in older men.

Validation of the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale in older black and white women

OBJECTIVES Despite routine use with older adults, the Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS) have not been adequately validated in older samples, particularly those from diverse racial backgrounds. The objective of this study was to determine the reliability and validity of and to provide normative data for these questionnaires in community-dwelling older women. METHODS Participants were 306 black and 2662 white women aged ≥70 from the Study of Osteoporotic Fractures. Participants completed the PSQI and ESS; provided self-reported assessments of mood, cognition and functioning; and underwent wrist actigraphy for sleep-wake estimation. RESULTS Good internal consistency in both black and white women was demonstrated for the PSQI and ESS. Two PSQI subscales, however, were found to have inadequate reliability (Medications and Daytime Dysfunction). Both the PSQI and ESS were associated with theoretically similar measures in the expected directions. The PSQI also differentiated participants with no reported sleep disorder from those reporting at least one sleep disturbance, such as insomnia, sleep apnea and restless legs. The ESS only differentiated women reporting no sleep disorder from those reporting insomnia. CONCLUSION In general, findings suggest that the PSQI and ESS are internally consistent, valid measures of self-reported sleep problems in older women. Additional research is required to evaluate the impact of removing the Medications and Daytime Dysfunction PSQI subscales on this measures internal consistency in older women.

Memory training interventions for older adults: A meta-analysis

A systematic review and meta-analysis of memory training research was conducted to characterize the effect of memory strategies on memory performance among cognitively intact, community-dwelling older adults, and to identify characteristics of individuals and of programs associated with improved memory. The review identified 402 publications, of which 35 studies met criteria for inclusion. The overall effect size estimate, representing the mean standardized difference in pre-post change between memory-trained and control groups, was 0.31 standard deviations (SD; 95% confidence interval (CI): 0.22, 0.39). The pre-post training effect for memory-trained interventions was 0.43 SD (95% CI: 0.29, 0.57) and the practice effect for control groups was 0.06 SD (95% CI: −0.05, 0.16). Among 10 distinct memory strategies identified in studies, meta-analytic methods revealed that training multiple strategies was associated with larger training gains (p = 0.04), although this association did not reach statistical significance after adjusting for multiple comparisons. Treatment gains among memory-trained individuals were not better after training in any particular strategy, or by the average age of participants, session length, or type of control condition. These findings can inform the design of future memory training programs for older adults.

Accuracy of Reports of Lifetime Mental and Physical Disorders: Results From the Baltimore Epidemiological Catchment Area Study

IMPORTANCE Our understanding of how mental and physical disorders are associated and contribute to health outcomes in populations depends on accurate ascertainment of the history of these disorders. Recent studies have identified substantial discrepancies in the prevalence of mental disorders among adolescents and young adults depending on whether the estimates are based on retrospective reports or multiple assessments over time. It is unknown whether such discrepancies are also seen in midlife to late life. Furthermore, no previous studies have compared lifetime prevalence estimates of common physical disorders such as diabetes mellitus and hypertension ascertained by prospective cumulative estimates vs retrospective estimates. OBJECTIVE To examine the lifetime prevalence estimates of mental and physical disorders during midlife to late life using both retrospective and cumulative evaluations. DESIGN, SETTING, AND PARTICIPANTS Prospective population-based survey (Baltimore Epidemiologic Catchment Area Survey) with 4 waves of interviews of 1071 community residents in Baltimore, Maryland, between 1981 and 2005. MAIN OUTCOMES AND MEASURES Lifetime prevalence of selected mental and physical disorders at wave 4 (2004-2005), according to both retrospective data and cumulative evaluations based on 4 interviews from wave 1 to wave 4. RESULTS Retrospective evaluations substantially underestimated the lifetime prevalence of mental disorders as compared with cumulative evaluations. The respective lifetime prevalence estimates ascertained by retrospective and cumulative evaluations were 4.5% vs. 13.1% for major depressive disorder, 0.6% vs. 7.1% for obsessive-compulsive disorder, 2.5% vs. 6.7% for panic disorder, 12.6% vs. 25.3% for social phobia, 9.1% vs. 25.9% for alcohol abuse or dependence, and 6.7% vs. 17.6% for drug abuse or dependence. In contrast, retrospective lifetime prevalence estimates of physical disorders ascertained at wave 4 were much closer to those based on cumulative data from all 4 waves. The respective prevalence estimates ascertained by the 2 methods were 18.2% vs. 20.2% for diabetes, 48.4% vs. 55.4% for hypertension, 45.8% vs. 54.0% for arthritis, 5.5% vs. 7.2% for stroke, and 8.4% vs. 10.5% for cancer. CONCLUSIONS AND RELEVANCE One-time, cross-sectional population surveys may consistently underestimate the lifetime prevalence of mental disorders. The population burden of mental disorders may therefore be substantially higher than previously appreciated.

The SBSM Guide to Actigraphy Monitoring: Clinical and Research Applications

The SBSM Guide to Actigraphy Monitoring: Clinical and Research Applications Sonia Ancoli-Israel, Jennifer L. Martin, Terri Blackwell, Luis Buenaver, Lianqi Liu, Lisa J. Meltzer, Avi Sadeh, Adam P. Spira & Daniel J. Taylor a Departments of Psychiatry and Medicine, University of California, San Diego b David Geffen School of Medicine at the University of California, Los Angeles c VA Greater Los Angeles Healthcare System, Geriatric Research, Education and Clinical Center d Research Institute, California Pacific Medical Center, San Francisco e Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine f Department of Psychiatry, University of California, San Diego g Department of Pediatrics, National Jewish Health, Denver h School of Psychological Sciences, Tel Aviv University, Israel i Department of Mental Health, Johns Hopkins Bloomberg School of Public Health j Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine k Department of Psychology, University of North Texas Published online: 14 Aug 2015.

Impact of Sleep on the Risk of Cognitive Decline and Dementia

Purpose of review Trouble falling or staying asleep, poor sleep quality, and short or long sleep duration are gaining attention as potential risk factors for cognitive decline and dementia, including Alzheimers disease. Sleep-disordered breathing has also been linked to these outcomes. Here, we review recent observational and experimental studies investigating the effect of poor sleep on cognitive outcomes and Alzheimers disease, and discuss possible mechanisms. Recent findings Observational studies with self-report and objective sleep measures (e.g. wrist actigraphy, polysomnography) support links between disturbed sleep and cognitive decline. Several recently published studies demonstrate associations between sleep variables and measures of Alzheimers disease pathology, including cerebrospinal fluid measures of A&bgr; and PET measures of A&bgr; deposition. In addition, experimental studies suggest that sleep loss alters cerebrospinal fluid A&bgr; dynamics, decrements in slow-wave sleep may decrease the clearance of A&bgr; from the brain, and hypoxemia characteristic of sleep-disordered breathing increases A&bgr; production. Summary Findings indicate that poor sleep is a risk factor for cognitive decline and Alzheimers disease. Although mechanisms underlying these associations are not yet clear, healthy sleep appears to play an important role in maintaining brain health with age, and may play a key role in Alzheimers disease prevention.

Neuropsychiatric Symptoms in Mild Cognitive Impairment: Differences by Subtype and Progression to Dementia

Neuropsychiatric symptoms (NPS) are common in patients with mild cognitive impairment (MCI). Little is known, however, about how NPS vary by MCI subtype (i.e. amnestic, single domain non‐memory, and multiple domain). In addition, it is unclear whether NPS increase risk of progression to dementia. We investigated the distribution of NPS across MCI subtypes and determined whether NPS increase risk of progression to dementia.