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      Sleep-Cognition Hypothesis In maritime Pilots, what is the effect of long-term work-related poor sleep on cognition and amyloid accumulation in healthy middle-aged maritime pilots: methodology of a case–control study

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          Abstract

          Introduction

          Evidence indicates a bidirectional relationship between poor sleep and Alzheimer’s disease (AD). While AD may lead to disruption of normal sleep, poor sleep in itself may play a causal role in the development of AD by influencing the production and/or clearance of the amyloid-beta (Aβ) protein. This led to the hypothesis that extended periods (>10 years) of sleep loss could lead to Aβ accumulation with subsequent cognitive AD-related decline. This manuscript describes the methodology of the SCHIP study, a cohort study in maritime pilots that aims at investigating the relationship between prolonged work-related sleep loss, cognitive function and amyloid accumulation among healthy middle-aged maritime pilots, to test the hypothesis that prolonged sleep loss increases the risk of AD-related cognitive decline.

          Methods

          Our study sample consists of a group of healthy middle-aged maritime pilots (n=20), who have been exposed to highly irregular work schedules for more than 15 years. The maritime pilots will be compared to a group of healthy, age and education-matched controls (n=20) with normal sleep. Participants will complete 10 days of actigraphy (Actiwatch 2, Philips Respironics) combined with a sleep-wake diary. They will undergo one night of polysomnography, followed by comprehensive assessment of cognitive function. Additionally, participants will undergo amyloid positron emission tomography-CT to measure brain amyloid accumulation and MRI to investigate atrophy and vascular changes.

          Analysis

          All analyses will be performed using IBM SPSS V.20.0 (SPSS). We will perform independent samples t-tests to compare all outcome parameters.

          Ethics and dissemination

          The study protocol was approved by our institutional ethical review board (NL55712.091.16, file number 2016–2337) and will be performed according to Good Clinical Practice rules. Data and results will be published in 2020.

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          Most cited references13

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          Sleep quality and 1-year incident cognitive impairment in community-dwelling older adults.

          To examine in cognitively intact older men and women the associations between subjective sleep quality and 1-yr incident cognitive impairment. Prospective cohort study. General community. 1,664 cognitively intact individuals age 65 to 96 years. 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. Sleep quality in older adults should receive particular attention by clinicians because poor sleep quality can be an early sign of cognitive decline.
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            Lifespan brain activity, β-amyloid, and Alzheimer's disease.

            Alzheimer's disease (AD) is the most common cause of progressive cognitive decline and dementia in adults. While the amyloid cascade hypothesis of AD posits an initiating role for the β-amyloid (Aβ) protein, there is limited understanding of why Aβ is deposited. A growing body of evidence based on in vitro, animal studies and human imaging work suggests that synaptic activity increases Aβ, which is deposited preferentially in multimodal brain regions that show continuous levels of heightened activation and plasticity across the lifespan. Imaging studies of people with genetic predispositions to AD are consistent with these findings, suggesting a mechanism whereby neural efficiency or cognitive reserve may diminish Aβ deposition. The aggregated findings unify observations from cellular and molecular studies with human cognitive neuroscience to reveal potential mechanisms of AD development. Copyright © 2011 Elsevier Ltd. All rights reserved.
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              Sleep disturbance is associated with incident dementia and mortality.

              People with Alzheimer' s disease (AD) commonly complain of sleep disturbances, which are seen in a wide variety of conditions that become more common in late life. It is not known whether sleep-related symptoms are associated with AD independently of their association with other illnesses. Secondary analyses of sleep-related measures collected through the Survey of Health, Ageing and Retirement in Europe (SHARE; i.e., sleeping problems, fatigue, taking sleeping medication, and trouble sleeping or a change in pattern) were conducted on those who reported the absence of AD or dementia at baseline. A 'sleep disturbance index' (SDI) using sleep-related measures was created and compared to a frailty index reflecting overall health status. Each sleep measure independently predicted self-reported AD or dementia and mortality within ~4 years. Combined, the SDI was associated with an increased risk of developing AD or dementia (OR= 1.23, 95%CI = 1.11-1.36) and mortality (OR = 1.18, 95% CI = 1.12-1.24), and remained a strong factor for dementia when overall health status was added to the risk model (p = 0.054). These findings indicate that sleep disturbance may exist prior to the manifestation of other typical symptoms observed in AD (e.g., memory loss). Sleep-related questions may be useful for screening individuals at risk for dementia and may allow for the earlier detection of AD at the preclinical stage.
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                Author and article information

                Journal
                BMJ Open
                BMJ Open
                bmjopen
                bmjopen
                BMJ Open
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                2044-6055
                2019
                27 June 2019
                : 9
                : 6
                : e026992
                Affiliations
                [1 ] departmentGeriatric Medicine , Radboudumc , Nijmegen, The Netherlands
                [2 ] Radboud Alzheimer Center , Nijmegen, The Netherlands
                [3 ] Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center , Nijmegen, The Netherlands
                [4 ] departmentNeurology , Radboudumc , Nijmegen, The Netherlands
                [5 ] departmentRadiology and Nuclear Medicine , Academic Medical Center , Amsterdam, The Netherlands
                [6 ] departmentRadiology and Nuclear Medicine , Radboudumc , Nijmegen, The Netherlands
                [7 ] Vincent van Gogh Institute for Psychiatry , Venray, The Netherlands
                [8 ] departmentMedical Psychology , Radboudumc , Nijmegen, The Netherlands
                [9 ] departmentEindhoven Medtech Innovation Center , Eindhoven University of Technology , Eindhoven, The Netherlands
                [10 ] Sleep Medicine Center Kempenhaeghe , Heeze, The Netherlands
                Author notes
                [Correspondence to ] Miss Jana Thomas; jana.thomas@ 123456radboudumc.nl
                Author information
                http://orcid.org/0000-0002-8249-7369
                http://orcid.org/0000-0001-9500-9793
                Article
                bmjopen-2018-026992
                10.1136/bmjopen-2018-026992
                6597630
                31248923
                59790b87-0805-425e-bfbe-6ecd61202b85
                © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

                This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

                History
                : 01 October 2018
                : 21 May 2019
                : 05 June 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100008398, Internationale Stichting Alzheimer Onderzoek;
                Categories
                Geriatric Medicine
                Protocol
                1506
                1698
                Custom metadata
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                Medicine
                alzheimer’s disease,amyloid accumulation,neurodegeneration,cognitive function,sleep
                Medicine
                alzheimer’s disease, amyloid accumulation, neurodegeneration, cognitive function, sleep

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