Polygenic risk for Alzheimer's disease predicts sleep slow-waves and daytime sleepiness in youth
By
Vincenzo Muto,
Ekaterina Koshmanova,
Pouya Ghaemmaghami,
Mathieu Jaspar,
Christelle Meyer,
Mahmoud Elansary,
Maxime Van Egroo,
Daphne Chylinski,
Christian Berthomier,
Marie Brandewinder,
Charlotte Mouraux,
Christina Schmidt,
Gregory Hammad,
Wouter Coppieters,
Naima Ahariz,
Christian Degueldre,
Andre Luxen,
Eric Salmon,
Christophe Phillips,
Simon N Archer,
Loic Yengo,
Enda Byrne,
Fabienne Collette,
Michel Georges,
Derk-Jan Dijk,
Pierre Maquet,
Peter M. Visscher,
Gilles Vandewalle
Posted 27 Feb 2020
medRxiv DOI: 10.1101/2020.02.26.20027912
Sleep disturbances and genetic variants have been identified as risk factors for Alzheimers disease. Whether genome-wide polygenic risk scores (PRS) for AD associate with sleep phenotypes in young adults, decades before typical AD symptom onset, is currently not known. We extensively phenotyped sleep under different sleep conditions and compute whole-genome Polygenic Risk Scores (PRS) for AD in a carefully selected homogenous sample of healthy 363 young men (22.1 y {+/-} 2.7) devoid of sleep and cognitive disorders. AD PRS was associated with more slow wave energy, i.e. the cumulated power in the 0.5-4 Hz EEG band, a marker of sleep need, during habitual sleep and following sleep loss. Furthermore higher AD PRS was correlated with higher habitual daytime sleepiness. These results imply that sleep features may be associated with AD liability in young adults, when current AD biomarkers are typically negative, and reinforce the idea that sleep may be an efficient intervention target for AD.
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