Common Sleep Aid Linked to Lower Alzheimer’s Protein Buildup

Despite the extensive research surrounding Alzheimer’s disease, numerous enigmatic aspects remain, particularly the intriguing correlation between inadequate sleep and the advancement of the disease, a connection that has garnered significant scholarly interest.

A recent study, published in 2023, elucidates that the administration of hypnotic medications can mitigate the accumulation of deleterious protein aggregates in the cerebrospinal fluid, which plays a crucial role in the brain’s nightly cleansing process.

Researchers affiliated with Washington University in St. Louis discovered that participants who ingested suvorexant, a widely used insomnia treatment, for merely two nights at a sleep clinic exhibited a modest reduction in the levels of two pivotal proteins—amyloid-beta and tau—which are notorious for their role in the pathology of Alzheimer’s.

Although the study’s short duration and limited sample comprised only healthy adults devoid of cognitive impairments, it offers compelling insights into the nexus between sleep quality and Alzheimer’s-related molecular markers.

Sleep disturbances often serve as precursors to Alzheimer’s, manifesting long before cognitive decline becomes apparent. By the time initial symptoms arise, levels of abnormal amyloid-beta are typically near their zenith, forming plaques that obstruct neuronal function.

Researchers posit that enhancing sleep quality may be a promising strategy for potentially delaying the onset of Alzheimer’s by facilitating the brain’s ability to cleanse itself of residual proteins and other metabolic waste.

Nonetheless, caution is warranted; neurologist Brendan Lucey of Washington University’s Sleep Medicine Center warns against interpreting these findings as a rationale for habitual suvorexant use among individuals harboring concerns about Alzheimer’s. The study’s brevity and the small cohort necessitate a prudent perspective on the therapeutic use of sleeping pills.

Despite the potential advantages, prolonged reliance on sleeping medications poses risks of dependency and may induce suboptimal sleep architecture, undermining the restorative benefits of deep sleep phases. Prior investigations have highlighted a correlation between diminished quality of slow-wave sleep and elevated levels of tau tangles and amyloid-beta.

Future research, particularly involving older populations over extended periods, is crucial in assessing the long-term efficacy of sleeping aids on protein levels while weighing their potential drawbacks.

Fundamentally, the prevailing hypothesis surrounding Alzheimer’s disease, which implicates aberrant protein aggregation in its pathophysiology, is currently facing rigorous scrutiny. Despite the years of research aimed at reducing amyloid levels yielding limited therapeutic success, the relationship between sleep disturbances and Alzheimer’s becomes increasingly compelling amidst the broader quest to elucidate the disease’s etiology.

In summary, while the prospective application of sleeping medications as a preventative measure against Alzheimer’s remains speculative, maintaining proper sleep hygiene and addressing sleep disorders can significantly enhance overall brain health.

“I remain hopeful for the development of pharmacological interventions that leverage the relationship between sleep and Alzheimer’s to stymie cognitive decline,” remarks Lucey, albeit acknowledging that we have yet to reach a definitive solution.

The findings are published in the Annals of Neurology.

An earlier version of this article was published in April 2023.