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Coulthard, E.

Publications and source records attributed to Coulthard, E..

2 recordsLinked to original sources

Is disrupted sleep a risk factor for Alzheimers disease? Evidence from a two-sample Mendelian randomization analysis

INTRODUCTIONIt is established that Alzheimers disease (AD) patients experience sleep disruption. However, it remains unknown whether disruption in the quantity, quality or timing of sleep is a risk factor for the onset of AD.\n\nMETHODSMendelian randomization (MR) was used to estimate the causal effect of self-reported and accelerometer-measured sleep parameters (chronotype, duration, fragmentation, insomnia, daytime napping and daytime sleepiness) on AD risk.\n\nRESULTSOverall, there was little evidence that sleep traits affect the risk of AD. There was some evidence to suggest that self-reported daytime napping was associated with lower AD risk (odds ratio [OR]: 0.70, 95% confidence interval [CI]: 0.50 to 0.99). Some other sleep traits (accelerometer-measured eveningness and sleep duration, and self-reported daytime sleepiness) had ORs for AD risk of a similar magnitude to daytime napping, but were less precisely estimated.\n\nDISCUSSONOur findings provide tentative evidence that daytime napping may reduce AD risk. However, findings should be replicated using independent samples.

epidemiology

Measuring the relationship between sleep, physical activity and cognition

Biochemical and neuropsychological changes due to poor sleep may contribute to the development of neurodegenerative disorders, such as dementia. Physical activity is widely thought to improve sleep; however, the optimal intensity/duration of physical activity required is unknown. This 14-week, single-blind study (n=23) investigated the feasibility of a self-directed physical activity intervention in healthy adults using actigraphy and cognitive function measures as primary outcomes. Participants were randomised to a control group (no change in routine) or the intervention group (increased physical activity) and were provided with an actigraphy device to monitor activity. Participants completed daily sleep/activity diaries and three cognitive assessment sessions. Vigorous physical activity increased between baseline and week 3 for the intervention group only, with no identifiable impact on sleep. This change was not sustained at week 12. Performance on an executive function task and delayed visuospatial recall improved from baseline to week 12 for the intervention group only. Contrary to our expectations, increasing light-moderate physical activity was associated with more impaired sleep across all participants. It is clear that the relationships between physical activity, sleep and cognition are complex and require further investigation. We discuss optimal methodologies for clinical trials investigating physical activity and/or sleep interventions targeting cognition.

neuroscience