4.6 Article

Self-reported sleep relates to microstructural hippocampal decline in ss-amyloid positive Adults beyond genetic risk

Journal

SLEEP
Volume 44, Issue 11, Pages -

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/sleep/zsab110

Keywords

hippocampus; sleep; beta-amyloid; Alzheimer's disease; memory; aging; lifespan; longitudinal; mean diffusivity

Funding

  1. EU [732592]
  2. European Research Council [283634, 725025, 313440, 677804]
  3. Norwegian Research Council
  4. National Association for Public Health's dementia research program, Norway
  5. Knut and Alice Wallenberg (KAW) foundation
  6. Spanish Ministry of Science, Innovation and Universities (MICIUN) grant [RTI2018-095181-B-C21]
  7. ICREA Academia 2019 Award
  8. Walnuts and Healthy Aging - California Walnut Commission, Sacramento, California
  9. German Federal Ministry of Education and Research [16SV5537/16SV5 837/16SV5538/16SV5536K/01UW0808/01UW0706/01GL1716A/01 GL1716B]
  10. Lifelong Health and Well-being Programme Grant from the UK Medical Research Council [G1001354]

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The study found that poor sleep quality and low sleep efficiency were associated with a faster decline in hippocampal microstructure, especially in the presence of A beta accumulation. The decline in hippocampal integrity mediated the relationship between sleep efficiency and memory decay.
Study Objectives: A critical role linking sleep with memory decay and beta-amyloid (A beta) accumulation, two markers of Alzheimer's disease (AD) pathology, may be played by hippocampal integrity. We tested the hypotheses that worse self-reported sleep relates to decline in memory and intra-hippocampal microstructure, including in the presence of A beta. Methods: Two-hundred and forty-three cognitively healthy participants, aged 19-81 years, completed the Pittsburgh Sleep Quality Index once, and two diffusion tensor imaging sessions, on average 3 years apart, allowing measures of decline in intra-hippocampal microstructure as indexed by increased mean diffusivity. We measured memory decay at each imaging session using verbal delayed recall. One session of positron emission tomography, in 108 participants above 44 years of age, yielded 23 A beta positive. Genotyping enabled control for APOE epsilon 4 status, and polygenic scores for sleep and AD, respectively. Results: Worse global sleep quality and sleep efficiency related to more rapid reduction of hippocampal microstructure over time. Focusing on efficiency (the percentage of time in bed at night spent asleep), the relation was stronger in presence of A beta accumulation, and hippocampal integrity decline mediated the relation with memory decay. The results were not explained by genetic risk for sleep efficiency or AD. Conclusions: Worse sleep efficiency related to decline in hippocampal microstructure, especially in the presence of A beta accumulation, and A beta might link poor sleep and memory decay. As genetic risk did not account for the associations, poor sleep efficiency might constitute a risk marker for AD, although the driving causal mechanisms remain unknown.

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