Poor sleep may predict Alzheimer’s onset years before symptoms appear
A robust new study from researchers at UC Berkeley has found a consistent association between poor sleep and greater accumulation of the toxic proteins thought to be the pathological cause of Alzheimer’s disease. The researchers suggest fragmented sleep could be an effective early way to predict those most at risk of developing the neurodegenerative disease.
An impressive volume of study over the past few years has homed in on the relationship between sleep and neurodegenerative disease. Irregular and fragmented sleep is a well-known symptom of Alzheimer’s disease and some researchers are beginning to suggest poor sleep may not just be a consequence of the neurodegeneration associated with the disease, but a potential cause as well.
Animal and human studies have effectively demonstrated as little as one night of disrupted sleep can increase accumulations of the toxic proteins associated with Alzheimer’s disease. Researchers have also homed in on the deep slow-wave phase of sleep as a key mechanism our brains utilize to clear our toxic proteins.
“We know there’s a connection between people’s sleep quality and what’s going on in the brain, in terms of Alzheimer’s disease,” says lead author on the new study, Joseph Winer. “But what hasn’t been tested before is whether your sleep right now predicts what’s going to happen to you years later. And that’s the question we had.”
The researchers recruited 32 cognitively healthy adults in their mid-70s, all who initially participated in an overnight sleep-lab stay allowing the researchers to record baseline sleep behaviors. Over the next few years the subjects periodically completed PET scans tracking the growth of amyloid plaques in their brains.
A clear correlation was identified between the subjects’ baseline sleep quality and accumulation of amyloid plaques over the subsequent few years. In particular, the results suggest fragmented sleep and lower volumes of non-REM slow-wave sleep signaled the greatest increases in amyloid plaque build-up.
“We have found that the sleep you’re having right now is almost like a crystal ball telling you when and how fast Alzheimer’s pathology will develop in your brain,” says Matthew Walker, senior author on the new study. “Measuring sleep effectively helps us travel into the future and estimate where your amyloid buildup will be.”
It is important to note, the new study only examined cognitively healthy older adults. So while the research does offer evidence disrupted sleep can predict amyloid plaque accumulations in the future, it does not provide evidence these particular aggregations directly lead to the development of Alzheimer’s, or even mild dementia.
The next steps for the research will be to investigate whether interventions to improve sleep quality can directly influence the rate of amyloid plaque accumulation. Longer-term studies will also be necessary to understand whether Alzheimer’s risk can be reduced by improving sleep behavior in middle-aged subjects.
“Our hope is that if we intervene, then in three or four years the buildup is no longer where we thought it would be because we improved their sleep,” says Winer. “If deep, restorative sleep can slow down this disease, we should be making it a major priority. And if physicians know about this connection, they can ask their older patients about their sleep quality and suggest sleep as a prevention strategy.”
The new study was published in the journal Current Biology.
Source: UC Berkeley