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Self-Reported Sleep Relates to Microstructural Hippocampal Decline in β-Amyloid Positive Adults Beyond Genetic Risk

By Håkon Grydeland, Donatas Sederevičius, Yunpeng Wang, David Bartrés-Faz, Lars Bertram, Valerija Dobricic, Sandra Düzel, Klaus P. Ebmeier, Ulman Lindenberger, Lars Nyberg, Sara Pudas, Claire E. Sexton, Cristina Solé-Padullés, Kristine B. Walhovd, Anders M. Fjell

Posted 28 Apr 2020
bioRxiv DOI: 10.1101/2020.04.28.061184

Background. To test the hypothesis that worse self-reported sleep relates to memory decay and reduced hippocampal integrity as indexed by increased intra-hippocampal water diffusion, and that the relations are stronger in the presence of β-amyloid (Aβ) accumulation, a marker of Alzheimer's disease (AD) pathology. Methods. Two-hundred and forty-three cognitively healthy participants, aged 19-81 years, completed the Pittsburgh Sleep Quality Index, and 2 diffusion tensor imaging sessions, on average 3 years apart, allowing measures of decline in hippocampal microstructural integrity as indexed by increased mean diffusivity. We measured memory decay using delayed recall from the California Verbal Learning Test. 18F-Flutemetamol positron emission tomography, in 108 participants above 44 years of age, yielded 23 Aβ positive. Genotyping enabled controlling for APOE ϵ4 status, and polygenic scores for sleep efficiency and AD. Results. Worse global sleep quality and sleep efficiency related to more rapid reduction in hippocampal microstructural integrity over time. Focusing on sleep efficiency, the relation was stronger in presence of Aβ accumulation. Sleep efficiency related to memory decay indirectly via hippocampal integrity decline. The results were not explained by genetic risk for sleep efficiency and AD. Conclusions. Poor self-reported sleep efficiency related to decline in hippocampal integrity, especially in the presence of Aβ accumulation. Poor sleep and hippocampal microstructural decline may partly explain memory decline in older adults with Aβ pathology. The relationships were not explained by genetic risk. Poor self-reported sleep efficiency might constitute a risk factor for AD, although the causal mechanisms driving the of observed associations remain unknown. ### Competing Interest Statement The authors have declared no competing interest.

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