Could prioritizing deep sleep be the key to protecting your brain? Scientists uncover how sleep disturbances may accelerate neurodegeneration—and why improving sleep could help delay cognitive decline.
Review: The night’s watch: Exploring how sleep protects against neurodegeneration. Image Credit: metamorworks / Shutterstock
Can better sleep help prevent or delay neurodegenerative diseases? Millions suffer from dementia worldwide, yet the relationship between sleep disturbances and cognitive decline remains complex.
In a recent review published in the journal Neuron, Washington University scientists explored whether disrupted sleep contributes to neurodegeneration, serves as an early symptom, or both. By understanding sleep’s protective mechanisms, they aimed to uncover ways to enhance brain health and resilience.
Sleep and brain health
Sleep restores brain function, consolidates memory, and removes toxic waste. However, as people age, sleep duration shortens, sleep becomes more fragmented, and deep sleep decreases—changes linked to cognitive decline and increased risk of neurodegenerative diseases.
Disruptions in non-rapid eye movement (NREM) sleep, particularly slow-wave sleep (SWS), are associated with early amyloid-beta (Aβ) plaque buildup and tau protein tangles, hallmarks of Alzheimer’s disease. Other neurodegenerative diseases, including Parkinson’s, Lewy body dementia, and frontotemporal dementia, often present with sleep disturbances years before cognitive symptoms appear.
Despite these associations, whether sleep disruptions drive neurodegeneration, reflect early pathology, or both remain uncertain. Understanding sleep’s role in brain health could lead to early interventions to delay or mitigate neurodegenerative diseases.
The current study
The researchers examined how sleep disruptions might contribute to cognitive decline, analyzing sleep patterns, brain activity, and molecular markers in both human and animal models.
They explored sleep architecture—especially changes in NREM and REM sleep—and their impact on neurodegenerative pathways. They also investigated sleep’s role in clearing metabolic waste, such as amyloid-beta and tau, but noted conflicting evidence on whether sleep consistently enhances clearance efficiency.
The study assessed how prolonged wakefulness and fragmented sleep affect neuronal activity, neuroinflammation, and brain homeostasis. Findings from animal models suggested that sleep deprivation accelerates neurodegeneration by increasing protein deposition and disrupting neuronal function.
Additionally, the study examined neurotransmitters like orexin, dopamine, and acetylcholine in regulating sleep-wake cycles and their influence on disease progression. Researchers also explored genetic predispositions to poor sleep, analyzing variants such as APOE4, DEC2, ABCA7, and TREM2 to determine their role in cognitive decline.
Key insights
The study found that disrupted sleep may contribute to neurodegeneration while also serving as an early symptom. Poor sleep was linked to increased accumulation of neurotoxic proteins, impaired clearance, and heightened neuronal activity, triggering inflammation and oxidative stress.
In both human and animal models, fragmented sleep and reduced slow-wave sleep correlated with early neurodegenerative changes. Those with genetic predispositions, such as APOE4 carriers, experienced more significant sleep disturbances and a higher dementia risk.
Different neurodegenerative disorders exhibited distinct sleep patterns. Alzheimer’s disease was associated with sleep fragmentation, while Parkinson’s and frontotemporal dementia often involved excessive daytime sleepiness and REM sleep behavior disorder.
Improving sleep—through behavioral changes, pharmacological interventions, or sleep therapies—mitigated neurodegenerative processes in experimental models. Enhancing slow-wave sleep reduced amyloid burden and improved cognitive function in animal studies.
However, researchers noted knowledge gaps, particularly in distinguishing causation from correlation in human studies. While sleep disturbances are linked to neurodegeneration, more research is needed to determine whether sleep interventions can delay disease onset.
Conclusions
The study reinforced the critical role of sleep in brain health, suggesting that sleep disturbances may accelerate neurodegeneration rather than just accompany it. Enhancing sleep quality, particularly deep sleep, could help protect against cognitive decline. Further research is needed to validate sleep-focused therapies in humans, but prioritizing sleep health may be essential in reducing neurodegenerative disease risk.