Older adults who don’t sleep well have more of the brain plaques that are hallmarks of Alzheimer’s disease, a new study suggests.
The finding doesn’t prove that not getting enough shut-eye causes the build-up of beta-amyloid plaques and leads to dementia rather than the other way around.
The researchers can’t be sure which came first because they asked about sleep problems and took brain images at around the same time.
But, the study’s lead author said, “It’s exciting that our findings … may point to sleep disturbance as something that can be a modifiable risk factor that can be leveraged to prevent Alzheimer’s disease.”
Adam Spira from the Johns Hopkins Bloomberg School of Public Health in Baltimore said past studies have found sleep quality is related to thinking and memory skills.
“We’ve known for a long time that people with Alzheimer’s disease have really disturbed sleep patterns,” he told Reuters Health. “People have wondered, well, is it possible that poor sleep is actually leading to cognitive decline?”
In the new study, “We were able to look under the hood and see what’s going on in the brain,” Spira said.
He and his colleagues asked 70 adults, ages 53 to 91 years, how many hours they slept each night and how often they woke up during the night or had otherwise disrupted sleep.
Then they scanned each person’s brain to look for clusters of beta-amyloid. The clumps of protein pieces are present in the brains of people with Alzheimer’s disease in much higher quantities than among healthy people.
The researchers wrote in JAMA Neurology that the amount of beta-amyloid plaques correlated with both the amount of sleep and sleep quality.
Average levels of beta-amyloid rose with every hour less that participants reported sleeping every night and with each additional point they scored on a question about poor sleep quality.
That was still true after Spira’s team took the four people who had developed cognitive impairment or Alzheimer’s disease during the study out of the equation.
Depending on the region of the brain they looked at, between one quarter and one third of the participants had higher than normal amounts of plaque.
Neurologist and sleep medicine researcher Dr. Yo-El Ju said the findings are consistent with other recent research.
“All of the studies so far are kind of showing the same thing, that there is an association between disrupted sleep and Alzheimer’s pathology, meaning brain changes,” Ju, from the Washington University School of Medicine in St. Louis, said.
None of those studies can prove which comes first, brain changes or sleep problems.
But research in animals suggests the link goes both ways: that sleep problems can drive the build-up of beta-amyloid and more beta-amyloid then contributes to worsening sleep, she told Reuters Health.
“At the very least it suggests that (sleep duration or fragmentation) may be a marker of an increased risk of developing Alzheimer’s disease, whether or not it’s the cause,” said Dr. Andrew Lim.
Lim is a neurologist at Sunnybrook Health Sciences Centre and the University of Toronto. He led a study in the same journal which found that getting plenty of sleep might be protective among people who have a gene that increases their risk of Alzheimer’s.
Ju, who wasn’t involved in either study, said everyone can benefit from sleeping better. And it never hurts to make sleep a priority.
Still, it’s “far too early” for people with poor sleep to be afraid they’re going to develop Alzheimer’s disease, she said.
Lim told Reuters Health the next step will be to follow people with sleep troubles over time to see if they develop brain plaques more quickly than others. If that’s the case, researchers could then test whether improving sleep might help prevent Alzheimer’s.
SOURCE: JAMA Neurology, online October 21, 2013.
Self-reported Sleep and β-Amyloid Deposition in Community-Dwelling Older Adults
Main Outcomes and Measures β-Amyloid burden, measured by carbon 11 – labeled Pittsburgh compound B positron emission tomography distribution volume ratios (DVRs).
Results After adjustment for potential confounders, reports of shorter sleep duration were associated with greater Aβ burden, measured by mean cortical DVR (B = 0.08 [95% CI, 0.03-0.14]; P = .005) and precuneus DVR (B = 0.11 [0.03-0.18]; P = .007). Reports of lower sleep quality were associated with greater Aβ burden measured by precuneus DVR (B = 0.08 [0.01-0.15]; P = .03).
Conclusions and Relevance Among community-dwelling older adults, reports of shorter sleep duration and poorer sleep quality are associated with greater Aβ burden. Additional studies with objective sleep measures are needed to determine whether sleep disturbance causes or accelerates Alzheimer disease.
Adam P. Spira, PhD; Alyssa A. Gamaldo, PhD; Yang An, MS; Mark N. Wu, MD, PhD; Eleanor M. Simonsick, PhD; Murat Bilgel, BS; Yun Zhou, PhD; Dean F. Wong, MD, PhD; Luigi Ferrucci, MD, PhD; Susan M. Resnick, PhD