Much like chicken soup, a good night’s sleep is good for the soul. And it’s not just a figurative lesson: sleep helps the brain process what it learned over the course of a day and clear toxic waste. Your glymphatic system—a relatively recently discovered network of tubes connecting the brain and bloodstream—replaces toxin-filled fluid with fresh liquid primarily during deep sleep. When this waste management system underperforms due to a lack of Z’s, it’s like when you forget to take the trash out to the curb. Once in a while, it’s not a big deal, but if you let it build up, your home (and by analogy, your brain) will start to experience all kinds of unrelated problems.
Alzheimer’s disease, a neurodegenerative disease characterized by the buildup of beta-amyloid and tau proteins, may be one such consequence of poor sleep. In a small proof-of-concept study, researchers at Washington University School of Medicine in St. Louis found that a pill used to treat insomnia lowered these Alzheimer’s-associated waste proteins, suggesting future preventative care for the disease focused on preserving and restoring good sleep. Their study was published on April 20 in the journal Annals of Neurology.
Brendan Lucey, the director of Washington University’s Sleep Medicine Center and the first author of the new research, said in a press release that the drug used in the study, a sleeping pill generically known as suvorexant, might be a promising way to impede the development of Alzheimer’s.
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“This drug is already available and proven safe, and now we have evidence that it affects the levels of proteins that are critical for driving Alzheimer’s disease,” he said.
In the study, Lucey and his team monitored 38 middle-aged participants for two nights in a sleep lab. After giving them no dose, a lower dose, or a higher dose of the sleeping medication at 9 p.m., participants were asked to sleep while researchers took samples of their brain and spinal fluid every two hours.
After a day and a half, participants who received the higher dose of suvorexant and got a good night’s sleep had 10-20 percent lower levels of beta-amyloid than participants who didn’t receive the medication. The proportion of phosphorylated tau protein—another marker of Alzheimer’s—was 10-15 percent lower in the high-dose group compared to the no-dose one.
These results are particularly encouraging when taken together with preliminary research suggesting consistently lowered levels of these waste proteins will make a difference in the long run, Lucey said.
“If we can lower amyloid every day, we think the accumulation of amyloid plaques in the brain will decrease over time,” he said.
Even so, a number of questions remain: Will chronic use of this drug maintain these benefits over time? It’s also known that neurodegenerative diseases like Alzheimer’s cause disruptions in sleep, creating a vicious cycle. It’s not yet known whether sleep-restoring treatment will be as effective for people in the throes of the disease, or provide significant benefits.
“I’m hopeful that we will eventually develop drugs that take advantage of the link between sleep and Alzheimer’s to prevent cognitive decline,” Lucey said. “We’re not quite there yet. At this point, the best advice I can give is to get a good night’s sleep if you can, and if you can’t, to see a sleep specialist and get your sleep problems treated.”
