STUDY OBJECTIVES To determine whether C-reactive protein (CRP), a marker of systemic inflammation, moderates the association between sleep and incident dementia. METHODS We studied Framingham Heart Study participants who completed at baseline a serum CRP assessment and in-home polysomnography to measure sleep duration, sleep efficiency, sleep latency, wake after sleep onset, number of awakenings, arousal index, and apnea-hypopnea index. Participants were divided into groups according to their CRP level: low (<1 mg/L), average (1-3 mg/L), high inflammation (>3 mg/L). Surveillance for outcomes (incident all-cause and Alzheimer's disease dementia) commenced at baseline and continued up to 22.5 years. RESULTS In 291 participants (mean age 67.5 ± 4.9 years, 51.6% men) followed for 13.4 ± 5.4 years, we observed 43 cases of all-cause dementia, 33 of which were clinically consistent with Alzheimer's disease. Whereas no direct association between CRP or sleep exposures was observed with incident dementia, CRP levels interacted with nighttime wakefulness when predicting both incident all-cause and Alzheimer's disease dementia. In the high CRP group, longer wake after sleep onset (hazard ratio [HR], 2.89; 95%CI, 1.31-6.34) and more nighttime awakenings (HR, 4.55; 95%CI, 1.19-17.38) were associated with higher risk of incident dementia. In the low CRP group, fewer nighttime awakenings were associated with a higher risk of incident dementia (HR, 0.07; 95%CI, 0.01-0.68). CONCLUSIONS Our findings suggest that inflammation moderates the association between sleep, particularly nighttime wakefulness, and dementia risk. The presence of inflammation may be an important determinant in evaluating how sleep disturbances relate to neurodegeneration.

中文翻译：

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全身炎症是睡眠和痴呆症之间的调节因素

研究目的 确定 C 反应蛋白 (CRP)（全身炎症标志物）是否调节睡眠与痴呆之间的关联。方法 我们研究了弗雷明汉心脏研究的参与者，他们在基线时完成了血清 CRP 评估和家庭多导睡眠图，以测量睡眠持续时间、睡眠效率、睡眠潜伏期、入睡后觉醒、觉醒次数、觉醒指数和呼吸暂停低通气指数。参与者根据 CRP 水平分为低组（<1 mg/L）、中组（1-3 mg/L）、高炎症组（>3 mg/L）。结果监测（全因事件和阿尔茨海默病痴呆）从基线开始，持续长达 22.5 年。结果 在 291 名参与者（平均年龄 67.5 ± 4.9 岁，51.6% 男性）中进行了 13.4 ± 5.4 年的随访，我们观察到 43 例全因痴呆病例，其中 33 例在临床上与阿尔茨海默病相符。虽然没有观察到 CRP 或睡眠暴露与痴呆症之间存在直接关联，但在预测全因痴呆症和阿尔茨海默氏病痴呆症时，CRP 水平与夜间觉醒存在相互作用。在高 CRP 组中，入睡后觉醒时间较长（风险比 [HR]，2.89；95%CI，1.31-6.34）和夜间觉醒次数较多（HR，4.55；95%CI，1.19-17.38）与较高风险相关痴呆症事件。在低 CRP 组中，夜间觉醒次数较少与痴呆发生风险较高相关（HR，0.07；95%CI，0.01-0.68）。结论我们的研究结果表明，炎症调节了睡眠（尤其是夜间清醒）与痴呆风险之间的关联。炎症的存在可能是评估睡眠障碍与神经退行性疾病之间关系的重要决定因素。