An intriguing study has revealed that improving sleep might offer benefits for brain health that scientists are just beginning to understand.
Researchers at Washington University in St. Louis discovered something remarkable: a common insomnia medication reduced levels of proteins associated with Alzheimer’s disease after just two nights of use.
This finding opens a fascinating window into how something as simple as better sleep might influence the biological processes linked to dementia. But before you call your doctor requesting a prescription, there’s much more to this story.
The Unexpected Connection
The study, published in the Annals of Neurology, found that participants who took suvorexant—a medication prescribed for insomnia—experienced a 10-20% reduction in amyloid-beta proteins circulating in their cerebrospinal fluid after just two nights.
These amyloid-beta proteins are the same ones that form the characteristic plaques clogging brain tissue in Alzheimer’s disease patients. Higher doses of the medication also temporarily reduced levels of hyperphosphorylated tau—another protein linked to Alzheimer’s progression and neuronal death.
“If you can reduce tau phosphorylation, potentially there would be less tangle formation and less neuronal death,” explained Dr. Brendan Lucey, director of Washington University’s Sleep Medicine Center, who led the research.
What makes this particularly interesting is that sleep disturbances aren’t just symptoms that appear after Alzheimer’s develops—they may actually be early warning signs that precede memory loss and cognitive decline. By the time those more recognizable symptoms emerge, abnormal protein levels are typically already approaching their peak.
How Sleep Cleans Your Brain
To understand why sleep matters so much for brain health, we need to look at what happens when we’re asleep.
During deep sleep phases, your brain undergoes something akin to a nightly cleaning service. Brain cells actually shrink slightly during sleep, creating wider channels for cerebrospinal fluid to flow through and flush away accumulated proteins and other waste products from the day’s neural activity.
This natural cleaning mechanism—sometimes called the glymphatic system—works most efficiently during deep, slow-wave sleep. When sleep is disrupted or insufficient, this crucial cleanup process may be compromised.
Previous research has shown that even one night of poor sleep can cause amyloid-beta levels to spike. This suggests that chronic sleep issues might allow these proteins to accumulate faster than the brain can clear them.
A Scientific Surprise
The Washington University team took an unusually direct measurement approach in their study. They recruited 38 middle-aged participants (45-65 years old) who showed no signs of cognitive impairment or sleep problems.
Researchers placed catheters to collect cerebrospinal fluid samples every two hours for 36 hours straight—through nighttime sleep, the following day, and another night. Participants randomly received either a clinical dose of suvorexant, a higher dose, or a placebo pill.
Here’s where things get interesting: despite the medication not significantly improving objective sleep quality measures between the groups, the protein levels still changed.
This suggests the medication might work through mechanisms beyond simply improving sleep—potentially acting directly on protein production or clearance pathways in the brain.
Even more curious, researchers observed the most significant drop in amyloid-beta with the standard clinical dose of suvorexant rather than the higher experimental dose. This counterintuitive finding suggests the relationship between the medication and protein levels isn’t a simple “more drug equals more effect” equation.
Why You Shouldn’t Run to Your Doctor (Yet)
Before these findings trigger a rush on sleep medication prescriptions, several important limitations deserve attention.
First, this was an extremely short study—just two nights—with a small sample of healthy individuals. Dr. Lucey explicitly warns that “it would be premature for people who are worried about developing Alzheimer’s to interpret it as a reason to start taking suvorexant every night.”
Long-term sleeping pill use carries significant risks:
- Physical and psychological dependence
- Rebound insomnia when stopping the medication
- Potentially suppressing crucial deep sleep phases
- Side effects including daytime drowsiness
- Increased fall risk, especially in older adults
The effect on tau protein was particularly fleeting. While levels dropped initially, they rebounded within 24 hours of taking the medication, suggesting any protection might be very temporary.
Additionally, the benefits observed in healthy middle-aged adults might not translate to older individuals already experiencing cognitive decline or those with diagnosed sleep disorders.
Rethinking Alzheimer’s
The entire premise connecting sleep medications to Alzheimer’s prevention rests on the amyloid hypothesis—the theory that abnormal protein buildup directly causes Alzheimer’s disease progression.
This long-dominant theory has faced increasing challenges in recent years. Decades of research targeting amyloid reduction have failed to produce effective treatments that actually slow cognitive decline in meaningful ways.
Many expensive clinical trials of drugs that successfully reduced amyloid plaques didn’t meaningfully improve patients’ symptoms or disease trajectory. This has prompted a significant rethinking of Alzheimer’s disease mechanisms.
While protein accumulation clearly correlates with the disease, the causal relationship is increasingly questioned—amyloid and tau might be markers or byproducts rather than primary drivers. If that’s the case, treatments focused solely on reducing these proteins might miss the actual disease mechanisms.
Better Sleep, Better Brain
Even if the protein-reduction effect proves less important than initially thought, improving sleep quality still offers numerous brain benefits beyond just protein clearance:
- Enhanced memory consolidation
- Reduced neuroinflammation
- Improved glucose metabolism in the brain
- Stabilized mood regulation
- Better stress hormone management
Dr. Lucey acknowledges this broader perspective, noting that “improving sleep hygiene and seeking treatment for sleep problems such as sleep apnea are both sensible approaches to improving general brain health at any age.”
The Future of Sleep Research
The Washington University team hopes to conduct longer studies examining whether sustained use of sleep medications produces lasting effects on protein levels in populations at higher risk for Alzheimer’s.
Researchers are also exploring non-pharmacological approaches to enhance sleep quality and specific sleep phases linked to better cognitive outcomes. These include:
- Acoustic enhancement techniques that strengthen slow-wave sleep
- Light therapy that helps regulate circadian rhythms
- Cognitive behavioral therapy for insomnia (CBT-I)
- Exercise protocols specifically designed to improve sleep architecture
- Meditation and stress-reduction techniques
The relationship between sleep disorders like obstructive sleep apnea and Alzheimer’s risk has become another major research focus. Some studies suggest treating sleep apnea might slow cognitive decline in people already showing early signs of dementia.
What You Can Do Right Now
While sleeping pills might eventually play a role in Alzheimer’s prevention strategies, current evidence suggests focusing on natural sleep improvement first:
Maintain consistent sleep schedules. Going to bed and waking up at the same times—even on weekends—helps regulate your body’s internal clock.
Create a proper sleep environment. Your bedroom should be dark, quiet, and cool (between 60-67°F).
Limit screen exposure before bed. The blue light from phones, tablets, and computers can suppress melatonin production.
Watch stimulant intake. Avoid caffeine after midday and limit alcohol, which might help you fall asleep but typically disrupts sleep quality.
Exercise regularly, but try to finish vigorous workouts at least 3-4 hours before bedtime.
Manage stress through techniques like meditation, deep breathing, or journaling before bed.
Seek treatment for sleep disorders like sleep apnea, restless leg syndrome, or clinical insomnia.
For those currently struggling with sleep issues, consulting a sleep specialist should take priority over self-medicating with over-the-counter sleep aids, which often provide limited benefit and can create dependence.
The Bottom Line
The Washington University study represents an early but promising step in understanding how sleep interventions might affect Alzheimer’s disease processes. While the results are intriguing, they remain preliminary.
“I’m hopeful that we will eventually develop drugs that take advantage of the link between sleep and Alzheimer’s to prevent cognitive decline,” said Dr. Lucey. “But we’re not quite there yet.”
The ideal approach might eventually combine targeted sleep medications with lifestyle modifications, perhaps alongside other emerging Alzheimer’s prevention strategies. For now, though, the most evidence-backed recommendation remains focusing on quality sleep through natural means—which benefits brain health in numerous ways beyond just protein clearance.
As research continues, the relationship between our nightly rest and long-term brain health grows clearer: quality sleep isn’t just about feeling refreshed tomorrow—it might be crucial for cognitive health decades later.
References
- Lucey, B.P., et al. (2023). “Effect of suvorexant on cerebrospinal fluid amyloid-β and tau kinetics in middle-aged healthy adults.” Annals of Neurology.
- Watson, C. (2025). “A Common Sleeping Pill Could Reduce Buildup of Alzheimer’s Proteins, Study Finds.” Health News.
- Winer, J.R., et al. (2022). “Association of Short and Long Sleep Duration With Amyloid-β Burden and Cognition in Aging.” JAMA Neurology.
- Holth, J.K., et al. (2019). “The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans.” Science.
- Spira, A.P., et al. (2018). “Sleep Duration and Subsequent Risk of Alzheimer’s Disease.” Current Opinion in Psychiatry.
