4.5 Article

Sleep Quality and Preclinical Alzheimer Disease

期刊

JAMA NEUROLOGY
卷 70, 期 5, 页码 587-593

出版社

AMER MEDICAL ASSOC
DOI: 10.1001/jamaneurol.2013.2334

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资金

  1. UCB
  2. Janssen Alzheimer Immunotherapy Program
  3. Pfizer
  4. National Institutes of Health (NIH) [P01-NS074969, P01-AG026276, P50-AG05681, P01-AG03991]
  5. Ellison Medical Foundation Senior Scholar Award
  6. National Center for Research Resources, a component of the NIH [UL1 RR024992]
  7. National Center for Research Resources, a component of the NIH Roadmap for Medical Research [UL1 RR024992]

向作者/读者索取更多资源

Importance: Sleep and circadian problems are very common in Alzheimer disease (AD). Recent animal studies suggest a bidirectional relationship between sleep and beta-amyloid (A beta), a key molecule involved in AD pathogenesis. Objective: To test whether A beta deposition in preclinical AD, prior to the appearance of cognitive impairment, is associated with changes in quality or quantity of sleep. Design: Cross-sectional study conducted from October 2010 to June 2012. Setting: General community volunteers at the Washington University Knight Alzheimer's Disease Research Center. Participants: Cognitively normal individuals (n=145) 45 years and older were recruited from longitudinal studies of memory and aging at the Washington University Knight Alzheimer's Disease Research Center. Valid actigraphy data were recorded in 142. The majority (124 of 142) were recruited from the Adult Children Study, in which all were aged 45 to 75 years at baseline and 50% have a parental history of late-onset AD. The rest were recruited from a community volunteer cohort in which all were older than 60 years and healthy at baseline. Main Outcome Measures: Sleep was objectively measured using actigraphy for 2 weeks. Sleep efficiency, which is the percentage of time in bed spent asleep, was the primary measure of sleep quality. Total sleep time was the primary measure of sleep quantity. Cerebrospinal fluid A beta 42 levels were used to determine whether amyloid deposition was present or absent. Concurrent sleep diaries provided nap information. Results: Amyloid deposition, as assessed by A beta 42 levels, was present in 32 participants (22.5%). This group had worse sleep quality, as measured by sleep efficiency (80.4% vs 83.7%), compared with those without amyloid deposition, after correction for age, sex, and APOE epsilon 4 allele carrier status (P=.04). In contrast, quantity of sleep was not significantly different between groups, as measured by total sleep time. Frequent napping, 3 or more days per week, was associated with amyloid deposition (31.2% vs 14.7%; P=.03). Conclusions and Relevance: Amyloid deposition in the preclinical stage of AD appears to be associated with worse sleep quality but not with changes in sleep quantity.

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