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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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