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Sleep problems have been associated with cognition, both cross-sectionally and longitudinally. Specific genes have been also associated with both sleep regulation and cognition. In a large group of older non-demented adults, we aimed to (a) validate the association between Sleep Polygenic Risk Score (Sleep PRS) and self-reported sleep duration, and (b) examine the association between Sleep PRS and cognitive changes in a three-year follow-up. Participants were drawn from the Hellenic Longitudinal Investigation of Aging and Diet (HELIAD). A structured, in-person interview, consisting of a medical history report and physical examination, was conducted for each participant during each of the visits (baseline and first follow-up). In total, 1376 participants were included, having all demographic, genetic, and cognitive data, out of which, 688 had at least one follow-up visit. In addition, an extensive neuropsychological assessment examining five cognitive domains (memory, visuo-spatial ability, attention/speed of processing, executive function, and language) was administered. A PRS for sleep duration was created based on previously published, genome-wide association study meta-analysis results. In order to assess the relationship between the Sleep PRS and the rate of cognitive change, we used generalized estimating equations analyses. Age, sex, education, ApolipoproteinE-epsilon 4 genotype status, and specific principal components were used as covariates. On a further analysis, sleep medication was used as a further covariate. Results validated the association between Sleep PRS and self-reported sleep duration (B = 1.173, E-6, p = 0.001). Further, in the longitudinal analyses, significant associations were indicated between increased Sleep PRS and decreased visuo-spatial ability trajectories, in both the unadjusted (B = -1305.220, p = 0.018) and the adjusted for the covariates model (B = -1273.59, p = 0.031). Similarly, after adding sleep medication as a covariate (B = -1372.46, p = 0.019), none of the associations between Sleep PRS and the remaining cognitive domains were significant. PRS indicating longer sleep duration was associated with differential rates of cognitive decline over time in a group of non-demented older adults. Common genetic variants may influence the association between sleep duration and healthy aging/cognitive health.

Background: Sleep is implicated in cognitive functioning in young adults, while healthy older adults do not always demonstrate clear associations between sleep and cognitive functioning. Age‐related changes in sleep include a reduction in total sleep time and a greater incidence of sleep disorders, and are also an integral part of neurodegenerations. In the present study, we aimed to: a) identify common genetic variants that may influence self‐reported sleep duration, and b) examine the association between the identified genetic variants and performance in different cognitive domains. Method: A sample of 197 cognitively healthy participants, aged 20‐80 years, were selected from two study cohorts: The Reference Abilities Neural Network and the Cognitive Reserve. Each participant underwent an evaluation of sleep function and assessment of neuropsychological performance on four different domains (memory, speed of processing, fluid reasoning, language), and global cognition. Available imputed genome‐wide genotyped data was used to derive a Polygenic Risk Score (PRS) based on 69 genetic variants previously reported as associated with sleep duration. Multivariate linear models were used to test the associations between the PRS and sleep duration and cognitive performance. Age, sex, and education were used as covariates. Result: Higher PRS was linked to longer sleep duration and then, lower risk of poor performance in global cognition, fluid reasoning, speed of processing, and language, but was not associated with memory. Conclusion: We replicated the association between PRS and longer sleep duration. We additionally found a significant association between the PRS and cognitive function. Our results suggest that common genetic variants influence the link between sleep duration and cognitive health. Sleep duration may represent a potential causal pathway for cognition, and, thus, improving sleep habits might be as useful as a potential therapeutic target to improve cognitive performance. Funding: National Institute of Health (NIH)/ National Institute of Aging (NIA) [Grant numbers: R01 AG026158 and RF1 AG038465], and the Bodossakis foundation.

Subjective cognitive decline may reflect a dementia prodrome or modifiable risk factor such as sleep disturbance. What is the association between sleep and subjective cognitive decline? Cross-sectional design, from two studies of older adults: the WHICAP in the USA and the HELIAD in Greece. A total of 1,576 WHICAP and 1,456 HELIAD participants, without mild cognitive impairment, dementia or severe depression/anxiety, were included. Participants were mostly women, with 12 (WHICAP) and 8 (HELIAD) mean years of education. Sleep problems were estimated using the Sleep Scale from the Medical Outcomes Study. Subjective cognitive decline was assessed using a structured complaint questionnaire that queries for subjective memory and other cognitive symptoms. Multinomial or logistic regression models were used to examine whether sleep problems were associated with complaints about general cognition, memory, naming, orientation and calculations. Age, sex, education, sleep medication, use of medications affecting cognition, co-morbidities, depression and anxiety were used as co-variates. Objective cognition was also estimated by summarizing neuropsychological performance into composite z-scores. Sleep problems were associated with two or more complaints: WHICAP: β = 1.93 (95% confidence interval: 1.59–2.34), p ≤ .0001 HELIAD: β = 1.48 (95% confidence interval: 1.20–1.83), p ≤ .0001. Sleep problems were associated with complaints in all the cognitive subcategories, except orientation for the WHICAP. The associations were noted regardless of objective cognition. At any given level of objective cognition, sleep disturbance is accompanied by subjective cognitive impairment. The replicability in two ethnically, genetically and culturally different cohorts adds validity to our results. The results have implications for the correlates, and potential aetiology of subjective cognitive decline, which should be considered in the assessment and treatment of older adults with cognitive complaints. 28 5

18: 1543-1548. AIM: Although there is some evidence of the relationships between sleep duration/quality and nutrient and/or food intake, the associations between sleep and dietary patterns have been poorly explored. The aim of the present study was to evaluate sleep duration and quality in relation to adherence to the Mediterranean diet (MeDi), and to investigate the sex- and age-specific associations in a population-representative cohort of older adults. METHODS: Participants from the Hellenic Longitudinal Investigation of Aging and Diet were included. The sample consisted of 1639 adults aged ≥65 years. Sleep duration and quality were assessed through a self-report questionnaire, whereas adherence to the MeDi was evaluated by an a priori score. RESULTS: Sleep quality was positively associated with the MeDi in the unadjusted and the adjusted model (age, sex, depression, years of education, body mass index, level of physical activity and total energy intake were added as covariates). In contrast, sleep duration was not associated with MeDi adherence either in the unadjusted or the adjusted models. In relation to the age-related associations, sleep quality was positively associated with MeDi adherence in those aged ≤75 years, and not in those aged >75 years. Associations between sleep and MeDi did not differ between men and women. CONCLUSIONS: The present results suggest that sleep quality is associated with MeDi adherence in older adults there are also age-specific associations between sleep quality and the MeDi. Although additional studies are required, improvements in diet quality should be considered in the context of sleep management interventions in older individuals. Geriatr Gerontol Int 2018 18 11 1543 1548

BACKGROUND/AIMS: To examine the association between self-reported sleep problems and incidence of dementia in community-dwelling elderly people. METHODS: 1,041 nondemented participants over 65 years old were examined longitudinally. Sleep problems were estimated using the RAND Medical Outcomes Study Sleep Scale examining sleep disturbance, snoring, sleep short of breath or with a headache, sleep adequacy, and sleep somnolence. Cox regression analysis was used to examine the association between sleep problems and risk for incident dementia. Age, gender, education, ethnicity, APOE-ε4, stroke, heart disease, hypertension, diabetes, and depression were included as covariates. RESULTS: Over 3 years of follow-up, 966 (92.8%) participants remained nondemented, while 78 (7.2%) developed dementia. In unadjusted models, sleep inadequacy (’Get the amount of sleep you need’) at the initial visit was associated with increased risk of incident dementia (HR = 1.20; 95% CI 1.02-1.42; p = 0.027). Adjusting for all the covariates, increased risk of incident dementia was still associated with sleep inadequacy (HR = 1.20; 95% CI 1.01-1.42; p = 0.040), as well as with increased daytime sleepiness (’Have trouble staying awake during the day’) (HR = 1.24; 95% CI 1.00-1.54; p = 0.047). CONCLUSION: Our results suggest that sleep inadequacy and increased daytime sleepiness are risk factors for dementia in older adults, independent of demographic and clinical factors.