Yiallourou Stephanie, Baril Andree-Ann, Wiedner Crystal, Misialek Jeffrey R, Kline Christopher E, Harrison Stephanie, Cannon Ethan, Yang Qiong, Bernal Rebecca, Bisson Alycia, Himali Dibya, Cavuoto Marina, Weihs Antoine, Beiser Alexa, Gottesman Rebecca F, Leng Yue, Lopez Oscar, Lutsey Pamela L, Purcell Shaun M, Redline Susan, Seshadri Sudha, Stone Katie L, Yaffe Kristine, Ancoli-Israel Sonia, Xiao Qian, Vaou Eleni Okeanis, Himali Jayandra J, Pase Matthew P
School of Psychological Sciences & Turner Institute for Brain and Mental Health, Monash University, Australia.
Framingham Heart Study, MA, USA.
Sleep. 2025 May 16. doi: 10.1093/sleep/zsaf129.
Poor sleep may play a role in the risk of dementia. However, few studies have investigated the association between polysomnography (PSG)-derived sleep architecture and dementia incidence. We examined the relationship between sleep architecture and dementia incidence across five US-based cohort studies from the Sleep and Dementia Consortium (SDC).
Percent of time spent in stages of sleep (N1, N2, N3, REM sleep), wake after sleep onset, sleep maintenance efficiency, apnea hypopnea index and relative delta power were derived from a single night home-based PSG. Dementia was ascertained in each cohort using its cohort-specific criteria. Each cohort performed Cox proportional hazard regressions for each sleep exposure and incident dementia, adjusting for age, sex, body mass index, anti-depressant use, sedative use, and APOE e4 status. Results were then pooled in random effects model.
The pooled sample comprised 4,657 participants (30% women) aged ≥60 years (mean age was 74 years at sleep assessment). There were 998 (21.4%) dementia cases (median follow-up time of 5 to 19 years). Pooled effects of the five cohorts showed no association between sleep architecture and incident dementia. When pooled analysis was restricted to the three cohorts which had dementia case ascertainment based on DSM-IV/V criteria (n=2,374), higher N3% was marginally associated with an increased risk of dementia (HR: 1.06; 95%CI: 1.00-1.12, per percent increase N3, p=0.050).
There were no consistent associations between sleep architecture measured and the risk of incident dementia. Implementing more nuanced sleep metrics and examination of associations with dementia sub-types remains an important next step for uncovering more about sleep-dementia associations.
睡眠不佳可能在痴呆风险中起作用。然而，很少有研究调查多导睡眠图（PSG）得出的睡眠结构与痴呆发病率之间的关联。我们通过睡眠与痴呆症联盟（SDC）的五项美国队列研究，研究了睡眠结构与痴呆发病率之间的关系。
从单次家庭PSG中得出睡眠各阶段（N1、N2、N3、快速眼动睡眠）所花费的时间百分比、睡眠开始后的觉醒时间、睡眠维持效率、呼吸暂停低通气指数和相对δ功率。每个队列使用其特定队列的标准确定痴呆症。每个队列针对每次睡眠暴露和新发痴呆症进行Cox比例风险回归，调整年龄、性别、体重指数、抗抑郁药使用、镇静剂使用和APOE e4状态。然后将结果汇总到随机效应模型中。
汇总样本包括4657名年龄≥60岁的参与者（30%为女性）（睡眠评估时的平均年龄为74岁）。有998例（21.4%）痴呆症病例（中位随访时间为5至19年）。五个队列的汇总效应显示睡眠结构与新发痴呆症之间无关联。当汇总分析仅限于根据DSM-IV/V标准确定痴呆症病例的三个队列（n = 2374）时，较高的N3%与痴呆症风险增加略有相关（HR：1.06；95%CI：1.00 - 1.12，N3每增加1%，p = 0.050）。
所测量的睡眠结构与新发痴呆症风险之间没有一致的关联。采用更细致的睡眠指标并检查与痴呆亚型的关联，仍然是进一步揭示睡眠与痴呆关联的重要下一步。
