Donders Institute for Brain, Cognition and Behaviour
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Thesis defense Jana Thomas(Donders series 458)

20 October 2020

Promotor: prof. dr. M. Olde Rikkert
Co-promotor: dr. J. Claassen

SLOW WAVES: Assessing sleep and detrimental effects of sleep disruption on brain amyloid-β and cognitive function in shift workers

In this thesis, we explored long-term effects of externally-induced sleep disruption on cognitive function, sleep quality, and brain amyloid-β load in different groups of shift workers (maritime pilots). Observations from previous studies showed that poor sleep could be one of the risk factors for AD-related processes through either less clearance or more production of amyloid-β during extended periods of wakefulness. These and other studies fueled the hypothesis that sleep disruption over the course of many years could increase amyloid-β concentrations, which could trigger AD-associated neurodegeneration and loss of cognitive function. Repeated nights of sleep disruption, as seen in the maritime pilot cohort, may contribute to the risk of AD by gradually increasing amyloid levels. We found that although maritime pilots report worse sleep quality during workweeks, they do not show deficits in cognitive function, no signs of global amyloid accumulation and no symptoms of early AD or MCI. Furthermore, the majority was able to readjust to a regular sleep behavior after >25 years of irregular sleep. Our results could be explained by the specific pattern, intensity and nature of sleep disruption in our cohort. We explored their sleep architecture with home-EEG measurements, which showed that even under less total sleep time and fragmented sleep during workweeks, the maritime pilots are able to generate sufficient amounts of slow wave sleep (deep sleep), which could act as a compensatory mechanism to counteract the detrimental effects of sleep disruption. Because we studied poor sleep as isolated variable, we further discussed other risk factors that, together with sleep disruption, could intensify AD risk, proposing an alternative hypothesis for the relationship between sleep and AD risk in which sleep loss might only increase AD risk in combination with other known risk factors.