PT  - JOURNAL ARTICLE
AU  - Anders M. Fjell
AU  - Øystein Sørensen
AU  - Inge K. Amlien
AU  - David Bartrés-Faz
AU  - Andreas M. Brandmaier
AU  - Nikolaus Buchmann
AU  - Ilja Demuth
AU  - Christian A Drevon
AU  - Sandra Düzel
AU  - Klaus P. Ebmeier
AU  - Paolo Ghisletta
AU  - Ane-Victoria Idland
AU  - Tim C. Kietzmann
AU  - Rogier A. Kievit
AU  - Simone Kühn
AU  - Ulman Lindenberger
AU  - Fredrik Magnussen
AU  - Didac Macià
AU  - Athanasia M. Mowinckel
AU  - Lars Nyberg
AU  - Claire E. Sexton
AU  - Cristina Solé-Padullés
AU  - Sara Pudas
AU  - James M. Roe
AU  - Donatas Sederevicius
AU  - Sana Suri
AU  - Didac Vidal-Piñeiro
AU  - Gerd Wagner
AU  - Leiv Otto Watne
AU  - René Westerhausen
AU  - Enikő Zsoldos
AU  - Kristine B. Walhovd
AU  - for the Alzheimer’s Disease Neuroimaging Initiative
TI  - Self-reported sleep problems are related to cortical thinning in aging but not memory decline and amyloid-β accumulation – results from the Lifebrain consortium
AID  - 10.1101/2020.04.28.065474
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.04.28.065474
4099  - http://biorxiv.org/content/early/2020/04/28/2020.04.28.065474.short
4100  - http://biorxiv.org/content/early/2020/04/28/2020.04.28.065474.full
AB  - Background Older persons with poor sleep are more likely to develop neurodegenerative disease, but the causality underlying this association is unclear. To move towards explanation, we examine whether sleep quality and quantity are similarly associated with brain changes across the adult lifespan.Methods Associations between self-reported sleep parameters (Pittsburgh Sleep Quality Index;PSQI) and longitudinal cortical change were tested using five samples from the Lifebrain consortium (n=2205, 4363 MRIs, 18-92 years). Analyses were augmented by considering episodic memory change, gene expression from the Allen Human Brain Atlas, and amyloid-beta (Aβ) accumulation (n=1980).Results PSQI components sleep problems and low sleep quality were related to thinning of the right lateral temporal cortex. The association with sleep problems emerged after 60 years, especially in regions with high expression of genes related to oligodendrocytes and S1 pyramidal neurons. BMI and symptoms of depression had negligible effects. Sleep problems were neither related to longitudinal change in episodic memory function nor to Aβ accumulation, suggesting that sleep-related cortical changes were independent of AD neuropathology and cognitive decline.Conclusion Worse self-reported sleep in later adulthood was associated with more cortical thinning in regions of high expression of genes related to oligodendrocytes and S1 pyramidal neurons, but not to Aβ accumulation or memory decline. The relationship to cortical brain change suggests that self-reported sleep parameters are relevant in lifespan studies, but small effect sizes, except for a few restricted regions, indicate that self-reported sleep is not a good biomarker of general cortical degeneration in healthy older adults.Competing Interest StatementClaire E Sexton reports consulting fees from Jazz Pharmaceuticals and is now a full-time employee of the Alzheimer’s Association. Christian A Drevon is a cofounder, stock-owner, board member and consultant in the contract laboratory Vitas AS, performing personalised analyses of blood biomarkers. The rest of the authors report no conflicts of interest.