We spend a significant portion of our lives in bed, and in recent years sleep research has uncovered considerable benefits to sleep not previously known.
One such study, recently published by investigators at the University of California (UC), Berkeley, suggests that defense against Alzheimer’s disease is deep, restorative sleep, and plenty of it. Specifically, the researchers found a way to estimate, with some degree of accuracy, a time frame for when Alzheimer’s is most likely to strike in a person’s lifetime.
“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,” explained co-senior study investigator Matthew Walker, PhD, a UC Berkeley professor of psychology and neuroscience, and director of the Center for Human Sleep Science. “The silver lining here is that there’s something we can do about it. The brain washes itself during deep sleep, and so there may be a chance to turn back the clock by getting more sleep earlier in life.”
Findings from the new study were published recently in Current Biology through an article titled “Sleep Disturbance Forecasts β-Amyloid Accumulation across Subsequent Years.”
In the current study, the Berkeley researchers matched the overnight sleep quality of 32 healthy older adults against the buildup in their brains of the toxic plaque known as beta-amyloid, a key player in the onset and progression of Alzheimer’s, which destroys memory pathways and other brain functions and afflicts more than 40 million people worldwide
“We tested the hypothesis that initial baseline measures of non-rapid eye movement (NREM) sleep slow-wave activity (SWA) and sleep quality (efficiency) provide future forecasting sensitivity to the rate of Aβ accumulation over subsequent years,” the authors wrote. “A cohort of clinically normal older adults was assessed using objective sleep polysomnography in combination with longitudinal tracking of Aβ accumulation with [11C]PiB positron emission tomography (PET) imaging. Both the proportion of NREM SWA below 1 Hz and the measure of sleep efficiency predicted the speed (slope) of subsequent Aβ deposition over time, and these associations remained robust when taking into account additional cofactors of interest (e.g., age, sex, sleep apnea).”
They found that the study participants who started out experiencing more fragmented sleep and less non-rapid eye movement (non-REM) slow-wave sleep were most likely to show an increase in beta-amyloid over the course of the study.
Although all participants remained healthy throughout the study period, the trajectory of their beta-amyloid growth correlated with baseline sleep quality. The researchers were able to forecast the increase in beta-amyloid plaques, which are thought to mark the beginning of Alzheimer’s.
“Rather than waiting for someone to develop dementia many years down the road, we are able to assess how sleep quality predicts changes in beta-amyloid plaques across multiple timepoints,” noted lead study investigator Joseph Winer, a PhD student in Walker’s lab. “In doing so, we can measure how quickly this toxic protein accumulates in the brain over time, which can indicate the beginning of Alzheimer’s disease.”
In addition to predicting the time it is likely to take for the onset of Alzheimer’s, the results reinforce the link between poor sleep and the disease, which is particularly critical in the face of the vast numbers of aging baby boomers.
Moreover, while previous studies have found that sleep cleanses the brain of beta-amyloid deposits, these new findings identify deep non-REM slow-wave sleep as the target of intervention against cognitive decline. And though genetic testing can predict one’s inherent susceptibility to Alzheimer’s, and blood tests offer a diagnostic tool, neither provides the potential for a lifestyle therapeutic intervention that sleep does, the researchers pointed out.
“If deep, restorative sleep can slow down this disease, we should be making it a major priority,” Winer said. “And if physicians know about this connection, they can ask their older patients about their sleep quality and suggest sleep as a prevention strategy.”
Throughout the multi-year study, the researchers periodically tracked the growth rate of the beta-amyloid protein in the participants’ brains using PET scans and compared the individuals’ beta-amyloid levels to their sleep profiles. The researchers focused on brain activity present during deep slow-wave sleep. They also assessed the study participants’ sleep efficiency, which is defined as actual time spent asleep, as opposed to lying sleepless in bed.
Amazingly, the results supported their hypothesis that sleep quality is a biomarker and predictor of disease down the road.
“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,” Winer remarked, “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.”
“Measuring sleep effectively helps us travel into the future and estimate where your amyloid buildup will be,” Walker added.
As for the next steps, Walker and Winer are looking at how they can take the study participants who are at high risk of contracting Alzheimer’s and implement methods that might boost the quality of their sleep.
“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,” Winer stated.
“Indeed, if we can bend the arrow of Alzheimer’s risk downward by improving sleep, it would be a significant and hopeful advance,” concluded Walker.