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26-05-2013 | Neurology | Article

Poor sleep quality possible marker of preclinical Alzheimer’s

Abstract

Free abstract

medwireNews: Researchers have found an association between poor sleep quality and amyloid deposition in the preclinical stage of Alzheimer's disease (AD).

They suggest that "sleep measures themselves could be used as markers of brain function, thereby facilitating faster and easier clinical trials of promising treatments in the preclinical and early clinical stages of AD."

David Holtzman (Washington University School of Medicine, St Louis, Missouri, USA) and colleagues used actigraphy to measure objective sleep quality over a 2-week period in 142 cognitively normal participants aged an average of 65.6 years. Of these, 32 (22.5%) had a cerebrospinal fluid (CSF) soluble β-amyloid (Aβ42) level of 500 pg/mL or less, indicating a high likelihood for amyloid deposition.

This group of patients had worse sleep quality, such that they spent a smaller percentage of time in bed asleep, at 80.4% versus 83.7% for those without amyloid deposition. This association was independent of age, gender, and apolipoprotein Eε4 carrier status.

By contrast, sleep quantity, measured as total sleep time, was not significantly associated with amyloid deposition.

But the researchers note in JAMA Neurology that a significantly higher percentage of patients with amyloid deposition took frequent naps (on 3 or more days a week), at 31.2% versus 14.7% of those without amyloid deposition.

They report a possible role for poor sleep efficiency in predicting amyloid deposition status. Using a cutoff of 75% for "poor" sleep efficiency and 89% for "good" sleep efficiency, Holtzman and team found that participants with poor sleep efficiency were 5.6 times more likely than those with good sleep efficiency to have amyloid deposition.

However, despite this strong trend, the association did not reach statistical significance, they note.

"We hypothesize that Aβ accumulation negatively affects sleep-wake behaviors, and conversely, poor sleep may increase risk of Aβ aggregation," they say.

The researchers add: "If sleep disruption increases risk of future AD, then this provides an even stronger motivation to identify and treat individuals with sleep disorders."

medwireNews (www.medwirenews.com) is an independent clinical news service provided by Springer Healthcare Limited. © Springer Healthcare Ltd; 2013

By Lucy Piper, Senior medwireNews Reporter

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