See the published version of this preprint at Alzheimer's Research and Therapy.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Recent evidence indicates that disrupted sleep could contribute to the development of Alzheimer’s disease by influencing the production and/or clearance of the amyloid-β protein. We set up a case-control study to investigated the association between long-term work-induced sleep disruption, cognitive function, and brain amyloid-β accumulation.
Methods: We recruited 19 male maritime pilots (aged 48-60 years) with chronic work-related sleep disruption and a sex-, age and education-matched control sample (n=16, aged 50-60 years) with normal sleep. Primary sleep disorders were ruled out with in-lab polysomnography. Additional sleep measurements were obtained at home using actigraphy, sleep-wake logs, and a single-lead EEG device. Cognitive function was assessed with a neuropsychological test battery sensitive to early symptomatic Alzheimer’s disease. Brain amyloid-β accumulation was assessed in maritime pilots using 18 F-flutemetamol amyloid PET-CT.
Results: Maritime pilots reported significantly worse sleep quality (Pittsburgh Sleep Quality Index (PSQI)=8.8±2.9) during workweeks, compared to controls (PSQI=3.2±1.4; 95% CI 0.01 to 2.57; p =0.049). This was confirmed with actigraphy-based sleep efficiency (86% ±3.8 vs. 89.3% ±4.3; 95% CI 0.43 to 6.03; p =0.03). Home-EEG recordings showed less total sleep time and deep sleep time during workweeks compared to rest-weeks (TST: 318.56 (250.21–352.93) vs. TST: 406.17 (340–425.98); p =0.001; DST: 36.75 (32.30–58.58) vs. DST 51.34 (48.37–69.30); p =0.005)). There were no differences in any of the cognitive domains between the groups. Abnormal amyloid-β accumulation was ruled out, showing mean global cortical standard uptake value ratios in the normal range (1.009 ±0.059; 95% CI 0.980 to 1.037), confirmed by visual reads.
Conclusions: Capitalizing on the particular work-rest schedule of maritime pilots, we show that long-term intermittent sleep disruption is not associated with brain amyloid accumulation or cognitive decline.
Keywords
sleep disruption, shift work, Alzheimer’s disease, amyloid-β, cognitive function
Figure 1
Figure 2
Figure 3
This is a list of supplementary files associated with this preprint. Click to download.
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Alzheimer's Research and Therapy.
No community comments so far
Editor assigned
On 22 Jun, 2020
Submission checks complete
On 21 Jun, 2020
Editor invited
On 21 Jun, 2020
Version 1
Posted 28 Apr, 2020
No comments provided
Reviewer #2 agreed
On 07 Jun, 2020
Review #2 received
Received 07 Jun, 2020
Editorial decision: Major Revision
On 07 Jun, 2020
Review #1 received
Received 19 May, 2020
Reviewer #1 agreed
On 02 May, 2020
Reviewers invited
Invitations sent on 01 May, 2020
Editor assigned
On 27 Apr, 2020
Editor invited
On 26 Apr, 2020
Submission checks complete
On 23 Apr, 2020
First submitted
On 21 Apr, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cognitive Neuroscience
Learn more about our company.
See the published version of this preprint at Alzheimer's Research and Therapy.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Alzheimer's Research and Therapy.
No community comments so far
Editor assigned
On 22 Jun, 2020
Submission checks complete
On 21 Jun, 2020
Editor invited
On 21 Jun, 2020
Version 1
Posted 28 Apr, 2020
No comments provided
Reviewer #2 agreed
On 07 Jun, 2020
Review #2 received
Received 07 Jun, 2020
Editorial decision: Major Revision
On 07 Jun, 2020
Review #1 received
Received 19 May, 2020
Reviewer #1 agreed
On 02 May, 2020
Reviewers invited
Invitations sent on 01 May, 2020
Editor assigned
On 27 Apr, 2020
Editor invited
On 26 Apr, 2020
Submission checks complete
On 23 Apr, 2020
First submitted
On 21 Apr, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cognitive Neuroscience
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Alzheimer's Research and Therapy.
Background: Recent evidence indicates that disrupted sleep could contribute to the development of Alzheimer’s disease by influencing the production and/or clearance of the amyloid-β protein. We set up a case-control study to investigated the association between long-term work-induced sleep disruption, cognitive function, and brain amyloid-β accumulation.
Methods: We recruited 19 male maritime pilots (aged 48-60 years) with chronic work-related sleep disruption and a sex-, age and education-matched control sample (n=16, aged 50-60 years) with normal sleep. Primary sleep disorders were ruled out with in-lab polysomnography. Additional sleep measurements were obtained at home using actigraphy, sleep-wake logs, and a single-lead EEG device. Cognitive function was assessed with a neuropsychological test battery sensitive to early symptomatic Alzheimer’s disease. Brain amyloid-β accumulation was assessed in maritime pilots using 18 F-flutemetamol amyloid PET-CT.
Results: Maritime pilots reported significantly worse sleep quality (Pittsburgh Sleep Quality Index (PSQI)=8.8±2.9) during workweeks, compared to controls (PSQI=3.2±1.4; 95% CI 0.01 to 2.57; p =0.049). This was confirmed with actigraphy-based sleep efficiency (86% ±3.8 vs. 89.3% ±4.3; 95% CI 0.43 to 6.03; p =0.03). Home-EEG recordings showed less total sleep time and deep sleep time during workweeks compared to rest-weeks (TST: 318.56 (250.21–352.93) vs. TST: 406.17 (340–425.98); p =0.001; DST: 36.75 (32.30–58.58) vs. DST 51.34 (48.37–69.30); p =0.005)). There were no differences in any of the cognitive domains between the groups. Abnormal amyloid-β accumulation was ruled out, showing mean global cortical standard uptake value ratios in the normal range (1.009 ±0.059; 95% CI 0.980 to 1.037), confirmed by visual reads.
Conclusions: Capitalizing on the particular work-rest schedule of maritime pilots, we show that long-term intermittent sleep disruption is not associated with brain amyloid accumulation or cognitive decline.
Figure 1
Figure 2
Figure 3
This is a list of supplementary files associated with this preprint. Click to download.
Loading...