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Preventing Alzheimer Disease in Your Sleep?

Preventing Alzheimer Disease in Your Sleep?

RESEARCH

With an aging population and subsequent predicted increase in incidence of Alzheimer disease (AD), identifying early markers and interventions is on the fast track. Research from the University of Wisconsin suggests that assessment of sleep quality and amyloid burden in midlife can identify AD risk and provide a window for early intervention.1

Previous research has correlated sleep problems with amyloid burden in seniors but not persons in late middle age in whom symptoms of cognitive decline have yet to emerge. Animal studies suggest that sleep disruption disrupts amyloid clearance, which is greatest during sleep.

Alzheimer prevention©OcskayMark/Shutterstock The researchers reasoned that sleep quality could be a useful therapeutic target for AD prevention because methods exist for improving sleep. They studied 98 cognitively healthy adults participating in the Wisconsin Registry for Alzheimer’s Prevention, a longitudinal cohort of more than 1500 cognitively healthy adults who were aged 40 to 65 years at study entry. Only those participants who had positron emission tomography (PET) scans and had completed the Epworth Sleepiness Scale and the Medical Outcomes Study Sleep Scale were included in the study. The average age of the study cohort was 62 years.

Amyloid binding was averaged within the 8 bilateral brain regions for which amyloid deposition and AD have been correlated (the angular gyrus, anterior cingulate gyrus, posterior cingulate gyrus, frontal medial orbital gyrus, precuneus, supramarginal gyrus, middle temporal gyrus, and superior temporal gyrus). Multiple regression analyses were used to examine the extent to which sleep scores predicted regional amyloid burden.

After adjusting for covariates, poorer sleep was significantly associated (P < .05) with greater amyloid burden particularly in the angular gyrus, frontal medial orbital cortex, cingulate gyrus, and precuneus. Although amyloid burden was associated with reportage of inadequate sleep, it was not associated with the amount of sleep reported, symptoms of sleep-disordered breathing, trouble falling asleep, or Epworth Sleepiness Scale scores.

The sleep measure most consistently associated with increased amyloid burden was the perception of less adequate sleep. This measure was derived from questions that asked participants whether they believed they were getting the amount of sleep they needed and enough sleep to feel rested. Also, the researchers did not diagnostically assess for sleep disorders; they only questioned participants on whether they had symptoms, and pointed out that many other studies have found an association between sleep-disordered breathing and dementia, including AD.

The bottom line
The researchers concluded that poor sleep may be a risk factor for AD and that sleep quality is a potential early marker or target for prevention during midlife. According to them, early interventions to improve sleep quality and treat sleep disorders could potentially slow down or prevent progression of AD by reducing amyloid pathology. In addition, sleep characteristics affected by amyloid deposition may act as biomarkers of preclinical AD and be useful in diagnosis, prognosis, and treatment monitoring. Prospective longitudinal studies and randomized control trials will be needed for further exploration of this issue.

References

1. Sprecher KE, Bendlin BB, Racine AM, et al. Amyloid burden is associated with self-reported sleep in nondemented late middle-aged adults. Neurobiol Aging. 2015 May 14. [Epub ahead of print]

 
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