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Preclinical amyloid deposition linked to poor sleep.

FROM JAMA NEUROLOGY

Preclinical beta-amyloid deposition in the brains of cognitively normal volunteers was associated with poor sleep quality but not sleep quantity, according to researchers.

"Our findings support the hypothesis that sleep-wake abnormalities are associated with the presence of amyloid deposition in the predinical stage of AD [Alzheimer's disease]," wrote Dr. Yo-El Ju of the Charles F. and Joanne Knight Alzheimer's Disease Research Center, Washington University, St. Louis, and her associates.

"Our findings may expand the temporal window during which sleep abnormalities are identifiable and potentially modifiable in AD," they noted.

Sleep-wake problems are common in AD, and early in its course, the disease affects brain regions and pathways important for sleep and wake mechanisms, Dr. Ju and her colleagues noted. "Even in mild cognitive impairment, or very mild dementia, there are abnormalities in sleep architecture and electroencephalography measures."

The researchers assessed the sleep of 142 volunteers aged 45-75 years (mean age, 66 years) using 2 weeks of actigraphy and sleep diary records. They recorded total sleep time, sleep efficiency (sleep time divided by time in bed), and wake time after sleep onset. Some had a parental history of symptomatic AD and were participating in longitudinal studies of healthy aging and dementia. All the subjects scored 0 on the Clinical Dementia Rating.

Overall, 32 participants (22.5%) had a cerebrospinal fluid level of amyloid beta 42 of less than 500 pg/mL, indicating a strong likelihood of amyloid deposition in the brain.

Those with a strong likelihood of amyloid deposition had significantly worse sleep efficiency (80.4% vs. 83.7%) than did those without amyloid deposition. This association remained significant after adjustment for age, sex, and apolipoprotein E epsilon-4 allele carrier status.

This difference in sleep efficiency also was significant in a subgroup analysis involving only the 100 study subjects who reported that their sleep had not changed during the preceding 5 years.

Wake time after sleep onset also was significantly higher (worse) among subjects with a strong likelihood of amyloid deposition than it was among those without it (63.1 min vs. 54 min).

In contrast, there were no differences between these two study groups in sleep quantity.

The participants with amyloid deposition showed a trend for spending more nonsleeping time in bed, but the trend didn't reach statistical significance. Similarly, they reported taking more naps per week, but the difference between the groups' average number of naps didn't reach statistical significance.

However, "when we looked at the proportion of frequent nappers, defined as those taking naps on 3 or more days per week, this was significantly higher in the group with amyloid deposition, compared with the group without amyloid deposition (31.2% vs. 14.7%)," Dr. Ju and her associates wrote (JAMA Neurol. 2013;70:587-93).

This study could not determine causality Amyloid deposition could cause sleep-wake disruption through several mechanisms, such as direct interference with neuronal function in areas of the brain that are critical for sleep. But poor sleep could just as well contribute to amyloid deposition, such as by increasing neuronal activity to a pathological degree, which is thought to facilitate deposition. It is likely that both of these processes play a role in a kind of positive feedback loop, the researchers said.

imnews@frontlinemedcom.com

Caption: Early in its course, AD affects brain regions and pathways important for sleep and wake mechanisms, researchers noted.

VITALS

Major finding: Study subjects with a strong likelihood of amyloid deposition had significantly worse sleep efficiency (80.4% vs. 83.7%) than did those without amyloid deposition.

Data source: A cross-sectional study of sleep abnormalities in 32 cognitively normal subjects who had preclinical amyloid deposition in the brain and 110 subjects who did not.

Disclosures: This study was supported by grants from the National Institutes of Health, the Ellison Medical Foundation Senior Scholar Award, and the National Center for Research Resources. Dr. Ju reported no financial conflicts of interest, but some of her associates reported ties to UCB, Jazz Pharmaceuticals, and other companies.
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Title Annotation:NEUROLOGY
Author:Moon, Mary Ann
Publication:Internal Medicine News
Date:Jun 1, 2013
Words:665
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