STUDY OBJECTIVES Sleep disturbances and genetic variants have been identified as risk factors for Alzheimer's disease. Our goal was to assess whether genome-wide polygenic risk scores (PRS) for AD associate with sleep phenotypes in young adults, decades before typical AD symptom onset. METHODS We computed whole-genome Polygenic Risk Scores (PRS) for AD and extensively phenotyped sleep under different sleep conditions, including baseline sleep, recovery sleep following sleep deprivation and extended sleep opportunity, in a carefully selected homogenous sample of healthy 363 young men (22.1 y ± 2.7) devoid of sleep and cognitive disorders. RESULTS 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, and potentially with large slow wave sleep rebound following sleep deprivation. Furthermore, higher AD PRS was correlated with higher habitual daytime sleepiness. CONCLUSIONS These results imply that sleep features may be associated with AD liability in young adults, when current AD biomarkers are typically negative, and the notion that quantifying sleep alterations may be useful in assessing the risk for developing AD.

中文翻译：

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阿尔茨海默病遗传风险和睡眠表型：与更多慢波和白​​天嗜睡有关

研究目标 睡眠障碍和遗传变异已被确定为阿尔茨海默病的危险因素。我们的目标是评估 AD 的全基因组多基因风险评分 (PRS) 是否与年轻人的睡眠表型相关，在典型的 AD 症状出现前几十年。方法 我们在精心挑选的 363 名健康年轻男性 (22.1 y ± 2.7) 没有睡眠和认知障碍。结果 AD PRS 与更多的慢波能量相关，即 0.5-4 Hz EEG 频带中的累积功率，这是在习惯性睡眠期间和睡眠缺失后睡眠需求的标志，并且可能在睡眠剥夺后出现大的慢波睡眠反弹。此外，较高的 AD PRS 与较高的习惯性白天嗜睡相关。结论 这些结果表明，当当前 AD 生物标志物通常为阴性时，睡眠特征可能与年轻人的 AD 易感性相关，并且量化睡眠改变的概念可能有助于评估发生 AD 的风险。