People who have trouble sleeping may be at greater risk for a variety of health problems, including being overweight and developing diabetes, heart disease or depression. Now add to the list memory problems.
Researchers at Washington University in St. Louis found that participants who had disrupted sleep — waking up repeatedly during the night — were more likely to show Alzheimer’s disease-related signs than sound sleepers. The researchers, led by neurologist Dr. Yo-El Ju, announced their results at the annual meeting of the American Academy of Neurology.
The study included 100 participants aged 45 to 80, half of whom had family histories of Alzheimer’s. The researchers monitored their sleep for two weeks and found that on average people spent a full 8 hours in bed each night, but only 6.5 hours sleeping, because they continued to wake up during the night.
Based on tests of participants’ spinal fluid and brain scans using PET and MRI imaging, Ju found that those who awoke more than five times per hour at night were more likely to have amyloid plaques in the brain, the hallmark of Alzheimer’s disease, compared with more restful sleepers. Participants with worse “sleep efficiency” — those who spent less than 85% of the time in bed asleep — were more likely to have preclinical Alzheimer’s disease.
The study is ongoing, so Ju says it’s not clear yet how the relationship works — whether amyloid starts to build up in the brain and then leads to poor sleep, or whether disrupted sleep triggers biological processes that contribute to amyloid deposits. Previous animal studies suggest that the connection is worth investigating, since mice bred to develop amyloid plaques tend to grow deposits earlier if they are sleep deprived, and animals that are given sleeping pills to help them slumber don’t get as many plaques.
“Which aspect specifically of sleep, and which stages of sleep are accounting for the change in brain activity is not known,” Ju says. She theorizes that deep sleep may slow the production of amyloid, leaving less for the brain to clear away during waking hours. That could explain why poor sleepers, who spend less time in deep sleep, tend to accumulate more of the nerve-damaging protein than those who sleep longer.
The results are only a preliminary look at what Ju hopes will be a comprehensive analysis of how the brain’s sleep-wake cycle may interact with the Alzheimer’s process. She and her team are in the process of recruiting more study volunteers and teasing apart whether risk factors such as family history or genes connected to Alzheimer’s could account for the relationship between sleep and memory problems.
Ju is hopeful that sleep modifying sleep patterns may be a useful way to lower patients’ risk of progressing from mild to more advances stages of the degenerative disease. Again, studies in mice support the possibility: animals that were bred to develop amyloid did not accumulate the protein when they were allowed to sleep more than they normally do.