Shireen Sindi1, Ingemar Kåreholt2, Lena Johansson3, Johan Skoog4, Linnea Sjöberg5, Hui-Xin Wang6, Boo Johansson7, Laura Fratiglioni8, Hilkka Soininen9, Alina Solomon10, Ingmar Skoog3, Miia Kivipelto11. 1. Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden; Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden; Neuroepidemiology and Ageing Research Unit, School of Public Health, Imperial College London, London, United Kingdom. Electronic address: shireen.sindi@ki.se. 2. Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden; Institute of Gerontology, School of Health and Welfare, Aging Research Network, Jönköping (ARN-J), Jönköping University, Jönköping, Sweden. 3. Institute of Neuroscience and Physiology, Center for Health and Ageing AGECAP, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. 4. Institute of Neuroscience and Physiology, Center for Health and Ageing AGECAP, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Psychology, Center for Health and Ageing AGECAP, University of Gothenburg, Gothenburg, Sweden. 5. Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden. 6. Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden; Stress Research Institute, Stockholm University, Stockholm, Sweden. 7. Department of Psychology, Center for Health and Ageing AGECAP, University of Gothenburg, Gothenburg, Sweden. 8. Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden; Stockholm Gerontology Research Center, Stockholm, Sweden. 9. Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland; Neurocenter, Neurology, Kuopio University Hospital, Kuopio, Finland. 10. Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden; Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland. 11. Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden; Neuroepidemiology and Ageing Research Unit, School of Public Health, Imperial College London, London, United Kingdom; Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland; Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland.
Abstract
INTRODUCTION: Few longitudinal studies assessed whether sleep disturbances are associated with dementia risk. METHODS: Sleep disturbances were assessed in three population-based studies (H70 study and Kungsholmen Project [Sweden]; Cardiovascular Risk Factors, Aging and Dementia study [Finland]). Late-life baseline analyses (3-10 years follow-up) used all three studies (N = 1446). Baseline ages ≈ 70 years (Cardiovascular Risk Factors, Aging and Dementia, H70), and ≈84 years (Kungsholmen Project). Midlife baseline (age ≈ 50 years) analyses used Cardiovascular Risk Factors, Aging and Dementia (21 and 32 years follow-up) (N = 1407). RESULTS: Midlife insomnia (fully adjusted hazard ratio = 1.24, 95% confidence interval = 1.02-1.50) and late-life terminal insomnia (fully adjusted odds ratio = 1.94, 95% confidence interval = 1.08-3.49) were associated with a higher dementia risk. Late-life long sleep duration (>9 hours) was also associated with an increased dementia risk (adjusted odds ratio = 3.98, 95% confidence interval = 1.87-8.48). DISCUSSION: Midlife insomnia and late-life terminal insomnia or long sleep duration were associated with a higher late-life dementia risk.
INTRODUCTION: Few longitudinal studies assessed whether sleep disturbances are associated with dementia risk. METHODS:Sleep disturbances were assessed in three population-based studies (H70 study and Kungsholmen Project [Sweden]; Cardiovascular Risk Factors, Aging and Dementia study [Finland]). Late-life baseline analyses (3-10 years follow-up) used all three studies (N = 1446). Baseline ages ≈ 70 years (Cardiovascular Risk Factors, Aging and Dementia, H70), and ≈84 years (Kungsholmen Project). Midlife baseline (age ≈ 50 years) analyses used Cardiovascular Risk Factors, Aging and Dementia (21 and 32 years follow-up) (N = 1407). RESULTS:Midlife insomnia (fully adjusted hazard ratio = 1.24, 95% confidence interval = 1.02-1.50) and late-life terminal insomnia (fully adjusted odds ratio = 1.94, 95% confidence interval = 1.08-3.49) were associated with a higher dementia risk. Late-life long sleep duration (>9 hours) was also associated with an increased dementia risk (adjusted odds ratio = 3.98, 95% confidence interval = 1.87-8.48). DISCUSSION: Midlife insomnia and late-life terminal insomnia or long sleep duration were associated with a higher late-life dementia risk.
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