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A study conducted by researchers at Washington University in St. Louis revealed that individuals who received suvorexant, a common insomnia treatment, for two nights at a sleep clinic experienced a slight reduction in two proteins -- amyloid-beta and tau -- associated with Alzheimer's disease.

Although the study was brief and encompassed a small cohort of healthy adults, it sheds light on the relationship between sleep patterns and the molecular indicators of Alzheimer's disease.

Sleep disturbances can serve as an early indicator of Alzheimer's disease, preceding symptoms such as memory loss and cognitive decline. By the time initial symptoms manifest, levels of abnormal amyloid-beta are typically elevated, forming plaques that obstruct brain cell function, Science Alert reported.

Researchers speculate that promoting healthy sleep may serve as a preventive measure against Alzheimer's disease, enabling the brain to eliminate accumulated proteins and metabolic waste during sleep.

However, neurologist Brendan Lucey, from Washington University's Sleep Medicine Center, who led the study, cautions against hasty conclusions saying, "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."

The study published in Annals of Neurology, spanned only two nights and involved 38 middle-aged participants without cognitive impairment or sleep disorders.

Extended use of sleeping pills is not an optimal remedy for individuals experiencing sleep deficits, as dependency can easily develop over time. Furthermore, these medications may induce lighter sleep phases rather than deeper ones, as evidenced by prior research linking decreased slow-wave sleep quality to heightened levels of tau tangles and amyloid-beta protein, according to findings from Lucey and colleagues.

In their most recent investigation, Lucey and associates sought to ascertain whether enhancing sleep quality with the assistance of sleeping pills could diminish levels of tau and amyloid-beta in the cerebrospinal fluid surrounding the brain and spinal cord. Previous studies have demonstrated that even a single night of disrupted sleep can lead to an increase in amyloid-beta levels.

A cohort of volunteers aged 45 to 65 received either one of two suvorexant doses or a placebo pill, administered an hour after researchers extracted a small sample of cerebrospinal fluid. Over the subsequent 36 hours, researchers collected samples every two hours while participants slept and throughout the following day and night to monitor changes in protein levels.

Despite comparable sleep patterns observed across all groups, individuals administered the suvorexant dose typically prescribed for insomnia experienced a notable reduction-between 10 and 20 percent-in amyloid-beta concentrations compared to those given a placebo.

The administration of a higher suvorexant dose also temporarily decreased levels of hyperphosphorylated tau, a modified version of the tau protein associated with the formation of tau tangles and subsequent cell death.

However, this effect was only observed for specific forms of tau, and tau concentrations rebounded within 24 hours following the ingestion of the sleeping pill.

Lucey expressed optimism saying, "If you can reduce tau phosphorylation, potentially there would be less tangle formation and less neuronal death." He emphasized the need for further research involving older adults and longer durations of sleeping pill use to uncover lasting effects on protein levels, while also taking into account possible downsides of these medications.

Nevertheless, mounting evidence suggests a connection between sleep disruptions and Alzheimer's disease, a condition lacking effective treatments. Lucey advocates for enhancing sleep hygiene and addressing sleep disorders like sleep apnea as prudent strategies for bolstering overall brain health across all age groups.

"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 Lucey. But he admitted, "We're not quite there yet."