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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阿尔茨海默氏病的遗传风险和睡眠表型：与更多的慢波和白天嗜睡相关

研究目标。睡眠障碍和遗传变异已被确定为阿尔茨海默氏病的危险因素。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（典型AD症状发作前数十年）的睡眠表型相关。方法。我们在精心挑选的健康363名年轻男性的同质样本中，计算了AD的全基因组多基因风险评分（PRS）和不同睡眠条件下的广泛表型睡眠，包括基准睡眠，睡眠剥夺后的恢复睡眠和延长的睡眠机会。 +/- 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，即在习惯性睡眠期间和失眠后0.5-4 Hz EEG频带中的累积功率（睡眠需求的标志）并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与较高的日间嗜睡度有关。结论。这些结果表明，当当前的AD生物标志物通常为阴性时，年轻人的睡眠特征可能与AD的不良反应有关，量化睡眠改变的概念可能有助于评估发展AD的风险。