A new study suggests that reduced sleep and poor sleep quality may be linked to increased build-up of beta-amyloid plaques in the brains of older adults – a sign of Alzheimer’s disease. This is according to a study published in the journal JAMA Neurology.
Researchers from The Johns Hopkins Bloomberg School of Health say that previous research has linked disturbed sleep to cognitive impairment in older individuals.
They note that those with Alzheimer’s disease (AD) have been shown to spend more time awake and have higher levels of fragmented sleep, compared with those who do not have the disorder.
Sleep patterns have previously been linked to beta-amyloid plaques. Research has indicated that changes in beta-amyloid levels may be regulated by sleep-wake patterns, the researchers say.
Therefore, they wanted to determine whether there is a link between beta-amyloid deposition and sleep variables within community-dwelling older adults.
The research team analyzed data from 70 adults with a mean age of 76 years, taken from the Baltimore Longitudinal Study of Aging. All participants were free of any form of dementia.
The participants were required to self-report their sleep patterns, disclosing the mean hours of sleep they had each night, how often they woke throughout the night, whether they had trouble falling asleep and whether they woke earlier than planned.
Their beta-amyloid deposition in the brain was measured using various brain imaging techniques.
The participants reported sleep duration ranging from no more than 5 hours, to more than 7 hours each night.
When comparing sleep duration with brain imaging showing the participant’s beta-amyloid deposition, it was found that shorter overall nights’ sleep duration and poor sleep quality were linked to increased beta-amyloid build-up.
However, the researchers note that the number of times a person woke during the night was not linked to an increase in beta-amyloid build-up.
The study authors say:
“Our results are consistent with those from animal research in which sleep deprivation increased interstitial fluid beta-amyloid levels.
These studies raise the possibility that poor sleep may promote beta-amyloid deposition, but they also raise questions about the mechanisms linking sleep/wake patterns and beta-amyloid burden.”
The researchers add that these findings could have significant public health implications, noting that AD is the most common form of dementia and almost half of older adults with the disorder report insomnia-based symptoms.
“Because late-life sleep disturbance can be treated, interventions to improve sleep or maintain healthy sleep among older adults may help prevent or slow AD to the extent that poor sleep promotes AD onset and progression,” the study authors say.
“This result would have a substantial effect on the independence and quality of life of older adults and their families and on the significant health care costs associated with AD.”
The researchers conclude that intervention trials are warranted in order to determine whether longer sleep duration and better sleep quality may prevent or slow the progression of Alzheimer’s disease.
Research into beta-amyloid deposition in the brain continues. Medical News Today reported earlier this month that researchers from the University of Rochester have suggested sleep “detoxes” the brain by flushing out the waste products of neural activity.
And another study by the University of Pittsburgh suggested that hardened arteries are linked to brain plaques.