A couple of nights of better sleep, helped along by a common insomnia drug, appeared to nudge down key Alzheimer’s-related proteins in a small 2023 study. The findings are preliminary, but they add to growing evidence linking poor sleep and the disease.
The study, published in Annals of Neurology, found healthy adults who took suvorexant for two nights had a slight drop in amyloid-beta and tau, two proteins that build up in Alzheimer’s disease.
Researchers from Washington University in St. Louis said the trial was short and involved only 38 middle-aged participants with no signs of cognitive impairment and no sleep problems.
Sleep disturbances can be an early warning sign of Alzheimer’s disease that appears before memory loss and cognitive decline. By the time the first symptoms develop, levels of abnormal amyloid-beta are almost peaking, forming clumps called plaques that clog brain cells.
Researchers think promoting sleep could help stave off Alzheimer’s disease by allowing the sleeping brain to flush leftover proteins and other waste products.
But lead author Brendan Lucey, a neurologist at Washington University’s Sleep Medicine Center, warned against reading too much into the results.
“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,” he said.
The study tested people aged 45 to 65, who received one of two doses of suvorexant or a placebo pill an hour after researchers collected a small sample of cerebrospinal fluid. Researchers then collected more samples every two hours for 36 hours while participants slept and during the next day and night.
There were no differences in sleep between the groups. Even so, amyloid-beta concentrations were reduced by between 10 and 20 percent with a dose of suvorexant usually prescribed for insomnia, compared to a placebo.
The higher dose also briefly lowered levels of hyperphosphorylated tau, a form of tau linked to tau tangles and cell death. But that effect showed up only in some forms of tau, and tau concentrations rose again within 24 hours of taking the drug.
“If you can reduce tau phosphorylation, potentially there would be less tangle formation and less neuronal death,” Lucey said.
The study also points to the limits of sleeping pills as a longer-term approach. The source text notes that prolonged use is not ideal because people can become dependent on them, and that sleeping pills may push people into shallower sleep rather than deep sleep phases.
That matters because earlier research from Lucey and colleagues found a link between lower-quality slow-wave sleep and higher levels of tau tangles and amyloid-beta protein. Past research has also shown that even one night of disrupted sleep can raise amyloid-beta levels.
The findings land amid broader questions about how Alzheimer’s disease develops. The leading theory, that abnormal protein clumps drive the disease, has faced scrutiny after decades of research aimed at lowering amyloid levels failed to produce a drug or therapy that prevents or slows Alzheimer’s disease.
Still, Lucey said improving sleep habits and treating sleep problems such as sleep apnea are sensible steps for general brain health.
“I’m hopeful that we will eventually develop drugs that take advantage of the link between sleep and Alzheimer’s to prevent cognitive decline,” Lucey said.
“But he admitted, “We’re not quite there yet.”
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