Beta-amyloid is a protein which is characteristically seen Alzheimer’s disease (AD). The findings are important because they suggest that helping people to get a good night’s sleep could prevent AD.
Previous research has already shown that AD risk could be reduced by modifying diet, exercise and cognitive activity.
However, sleep has not so far been found to be a risk factor, despite disturbed sleep being a hallmark of the disease.
It is thought that disturbed sleep patterns in patients with AD could be due to the growth of the amyloid plaques and resulting neuronal changes.
The long-term study was based on data acquired from the Baltimore Longitudinal Study of Aging (BLSA) that was initiated in 1958 by the National Institute on Aging (NIA).
The study was designed to monitor the long-term health of thousands of volunteers in order to discover risk factors for age-related conditions.
One of the components of this monitoring was a periodic questionnaire (from 1991 to 2000) which contained the questions: “Do you often become drowsy or fall asleep during the daytime when you wish to be awake?” and “Do you nap?”.
The first question required a yes/no response, while the second could be answered by “daily,” “1-2 times/week,” “3-5 times/week,” and “rarely or never.”
A smaller group of volunteers in this study began to undergo neuroimaging examinations in 1994, and some of them had PET (positron emission tomography) scans from 2005 onwards.
These scans used the radioactive Pittsburgh compound B (PIB) to pick up beta-amyloid deposits in the brain.
In total, 123 volunteers provided answers to the questions and also had a PET scan (after 16 years, on average).
Analysis of the data from this subgroup showed that those who answered “Yes” to daytime sleepiness had an unadjusted risk of beta-amyloid deposits which was three times greater than in those who answered “No”.
When the data was adjusted for factors such as age, sex, education and body-mass index which could affect daytime sleepiness, the risk still remained 2.75 times higher in the first group. This finding increases the possibility that AD could in part be caused by night-time sleep disturbances.
Volunteers who reported napping in the daytime also had a higher unadjusted risk, about twice as high, but this was not statistically significant.
The reason for this correlation is not known but could be due to the plaque-forming activity of daytime sleepiness itself.
The researchers also pointed out that the amyloid protein itself could conceivably be the cause of the daytime sleepiness, as well.
A more plausible reason is that sleep disturbances or lack of sleep promotes the formation of amyloid plaques, through an unknown mechanism, and also, obviously, cause the patient to experience daytime sleepiness.
Both animal and human studies have shown a linkage between poor or restricted night-time sleep and increased beta-amyloid protein deposits in the nervous system.
The results of the study suggest that the risk of AD could be reduced by appropriate intervention for individuals who have disturbed or insufficient sleep, whether this is treating sleep disorders such as obstructive sleep apnoea or insomnia, or modifying factors that act more broadly such as work-related sleep loss or poor sleep habits.
There is no cure yet for Alzheimer’s disease, so we have to do our best to prevent it… Prioritizing sleep may be one way to help prevent or perhaps slow this condition,” said Dr Adam P. Spira, Ph.D., Lead Investigator
The study, Excessive Daytime Sleepiness and Napping in Cognitively Normal Adults: Associations with Subsequent Amyloid Deposition Measured by PiB PET was carried out by researchers from the National Institute on Aging (NIA), the Bloomberg School and Johns Hopkins Medicine and reported recently in the journal SLEEP.
Source: News Medical Net