Belinda M Brown1,2, Stephanie R Rainey-Smith1,2, Victor L Villemagne3, Michael Weinborn1,2,4, Romola S Bucks4, Hamid R Sohrabi1,2, Simon M Laws1,2, Kevin Taddei1,2, S Lance Macaulay5, David Ames6,7, Christopher Fowler8, Paul Maruff8,9, Colin L Masters8, Christopher C Rowe3, Ralph N Martins1,2,10. 1. School of Medical Sciences, Edith Cowan University, Joondalup, Western Australia. 2. Sir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Nedlands, Western Australia. 3. Austin Health, Department of Nuclear Medicine and Centre for PET, Heidelberg, Victoria, Australia. 4. School of Psychology, University of Western Australia, Crawley, Western Australia. 5. CSIRO Food and Nutrition, Parkville, Victoria, Australia. 6. Department of Psychiatry, University of Melbourne, Victoria, Australia. 7. National Ageing Research Institute, Parkville, Victoria, Australia. 8. Florey Institute for Neurosciences and Mental Health, University of Melbourne, Victoria, Australia. 9. Cogstate Ltd., Melbourne, Victoria, Australia. 10. School of Psychiatry and Clinical Neurosciences, University of Western Australia, Nedlands, Western Australia.
Abstract
STUDY OBJECTIVES: To evaluate the association between self-reported sleep quality and levels of brain β-amyloid (Aβ) burden, and to determine the effect of the apolipoprotein E (APOE) ε4 allele on any associations found. METHODS: This study is a cross-sectional analysis of 184 cognitively healthy men and women aged over 60 y. We measured sleep quality factors: specifically, sleep duration, latency (time taken to fall asleep), disturbances, efficiency, daytime dysfunction, and overall sleep quality, using the Pittsburgh Sleep Quality Index. All participants underwent Aβ positron emission tomography imaging for the quantification of brain Aβ burden and were APOE genotyped. Linear regression analyses were used to evaluate the relationship between sleep quality factors and brain Aβ burden, adjusting for age, body mass index, cardiovascular disease, and symptoms of depression, with APOE ε4 carriage entered as a moderator. RESULTS: Of the sleep factors, longer sleep latency was associated with higher levels of brain Aβ (B = 0.003 [standard error = 0.001], P = 0.02). APOE ε4 allele (carrier/noncarrier) did not moderate the relationship between sleep latency and brain Aβ burden. CONCLUSIONS: Our findings suggest a relationship between brain Aβ burden and sleep latency, independent of APOE ε4 genotype.
STUDY OBJECTIVES: To evaluate the association between self-reported sleep quality and levels of brain β-amyloid (Aβ) burden, and to determine the effect of the apolipoprotein E (APOE) ε4 allele on any associations found. METHODS: This study is a cross-sectional analysis of 184 cognitively healthy men and women aged over 60 y. We measured sleep quality factors: specifically, sleep duration, latency (time taken to fall asleep), disturbances, efficiency, daytime dysfunction, and overall sleep quality, using the Pittsburgh Sleep Quality Index. All participants underwent Aβ positron emission tomography imaging for the quantification of brain Aβ burden and were APOE genotyped. Linear regression analyses were used to evaluate the relationship between sleep quality factors and brain Aβ burden, adjusting for age, body mass index, cardiovascular disease, and symptoms of depression, with APOE ε4 carriage entered as a moderator. RESULTS: Of the sleep factors, longer sleep latency was associated with higher levels of brain Aβ (B = 0.003 [standard error = 0.001], P = 0.02). APOE ε4 allele (carrier/noncarrier) did not moderate the relationship between sleep latency and brain Aβ burden. CONCLUSIONS: Our findings suggest a relationship between brain Aβ burden and sleep latency, independent of APOE ε4 genotype.
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