A 2023 study found that just two nights of a popular insomnia medication reduced levels of brain proteins linked to Alzheimer’s disease—but researchers urge caution about interpreting the results.
We spend roughly a third of our lives sleeping—or at least we should. But for millions with disturbed sleep patterns, that crucial recovery time falls short, potentially triggering numerous health problems beyond just daytime fatigue.
Now, a tantalizing connection between sleep medications and Alzheimer’s disease has emerged, offering a new perspective on how improving sleep might protect brain health.
The Sleep-Alzheimer’s Connection
Researchers at Washington University in St. Louis discovered that participants who took suvorexant—a medication commonly prescribed for insomnia—experienced a 10-20% reduction in amyloid-beta proteins circulating in their cerebrospinal fluid after just two nights.
These are the same proteins that form the characteristic plaques clogging brain tissue in Alzheimer’s disease.
The study also found that higher doses 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.
This insight offers an intriguing glimpse into how relatively simple interventions might affect the molecular markers of a disease that currently has no cure.
Sleep disturbances aren’t just a symptom of Alzheimer’s—they may actually be an early warning sign that appears before memory loss and cognitive decline set in. By the time these more recognizable symptoms develop, abnormal amyloid-beta levels are typically already approaching their peak.
Why Sleep Matters for Brain Health
The science behind this connection involves what happens when we sleep. During deep sleep phases, the brain undergoes something of a nighttime cleaning service.
Your 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 cleanup process may be compromised.
Previous studies have shown that even one night of poor sleep can cause amyloid-beta levels to spike. The research suggests that chronic sleep issues might allow these proteins to accumulate faster than the brain can clear them.
The Study’s Approach: Measuring Real-Time Changes
The Washington University team took a direct measurement approach. 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 of suvorexant
- A placebo pill
This continuous sampling allowed researchers to track protein level changes in real-time as the medication took effect.
But 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.
The conventional wisdom has been that better sleep equals better brain cleanup, but this study hints that specific sleep medications might have additional protective effects regardless of sleep quality improvement.
The researchers observed the most significant drop in amyloid-beta with the clinically prescribed 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.
The Limitations and Cautions
Before you rush to your doctor requesting a suvorexant prescription, several important caveats 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 and cognitive impairment
- 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.
The Alzheimer’s Theory Under Scrutiny
The entire premise connecting sleep interventions 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.
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.
Sleep as a Multipronged Brain Protector
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.”
Where Sleep Research Is Heading
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 without medications
- 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.
Practical Takeaways
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 or 15-19°C).
Limit screen exposure before bed. The blue light from phones, tablets, and computers can suppress melatonin production.
Watch your intake. Avoid caffeine after midday and limit alcohol, which might help you fall asleep but typically disrupts sleep quality.
Get regular exercise, 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 Future of Sleep-Based Treatments
The Washington University study represents an early step in understanding how sleep interventions might affect Alzheimer’s disease processes. While the results are promising, they’re 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.
