Common sleeping pill may reduce Alzheimer’s disease protein buildup, study finds: ScienceAlert

There’s still so much we don’t know about Alzheimer’s disease, but the link between lack of sleep and worsening disease is one that researchers are eagerly exploring.

Now, a new study has found that using sleeping pills to close your eyes could reduce the buildup of toxic protein clumps in the fluid that cleanses the brain each night.

Researchers from Washington University in St. Louis found that people who took suvorexant, a common treatment for insomnia, for two nights at a sleep clinic experienced a slight drop in two proteins, beta -amyloid and tau, which accumulate in Alzheimer’s disease.

Although short and involving a small group of healthy adults, the study is an interesting demonstration of the link between sleep and molecular markers of Alzheimer’s disease.

Sleep disturbances can be a warning sign of Alzheimer’s disease that precedes other symptoms, such as memory loss and cognitive decline. And by the time the first symptoms develop, levels of abnormal beta-amyloid nearly peak, forming clumps called plaques that clog brain cells.

Researchers believe that promoting sleep could be a way to stave off Alzheimer’s disease, by allowing the sleeping brain to empty itself of leftover proteins and other junk from the day.

Although sleeping pills can help in this regard, “it would be premature for people who fear developing Alzheimer’s disease to interpret this as a reason to start taking suvorexants every night,” says neurologist Brendan Lucey, from the University of Washington Center for Sleep Medicine, who led the research.

The study lasted just two nights and involved 38 middle-aged participants who showed no signs of cognitive impairment and had no problems sleeping.

Using sleeping pills for prolonged periods is also not an ideal solution for those who are sleep deprived, as it is quite easy to become addicted to them.

Sleeping pills can also lull people into shallower sleep episodes rather than deep sleep stages. This could be problematic because previous research by Lucey and her colleagues found a link between poorer quality, slow-wave sleep, and high levels of tau tangles and beta-amyloid protein.

In their latest study, Lucey and her colleagues wanted to see if improving sleep using sleeping pills could reduce levels of tau and beta-amyloid in the cerebrospinal fluid that bathes the brain and spinal cord. Previous research shows that even a single night of disrupted sleep can cause beta-amyloid levels to rise.

A group of volunteers between the ages of 45 and 65 were given one of two doses of suvorexant or a placebo pill, one hour after the researchers took their cerebrospinal fluid to collect a small sample.

The researchers continued to collect samples every two hours for 36 hours while the participants slept and during the following day and night, to measure changes in protein levels.

There was no difference in sleep between the groups, yet beta-amyloid levels were reduced by 10-20% with a dose of suvorexant usually prescribed for insomnia, compared to a placebo.

The higher dose of suvorexant also momentarily reduced levels of hyperphosphoryl tau, a modified form of tau protein linked to the formation of tau tangles and cell death.

However, this effect was only seen with certain forms of tau, and tau concentrations rose within 24 hours of taking the sleeping pill.

“If you could reduce tau phosphorylation, there would potentially be less tangle formation and less neuronal death,” says Lucey, still hoping that future studies in older adults testing sleeping pills for months could possibly measure a lasting effect on protein levels (while noting any downsides of sleeping pills).

Of course, all of this hinges on our understanding of the causes of Alzheimer’s disease.

The mainstream theory, that abnormal clumps of proteins cause Alzheimer’s disease, has come under intense scrutiny lately after decades of research aimed at reducing the levels of amyloid that have not resulted in a useful drug or therapy that actually prevents or slows the disease. This prompted researchers to rethink the development of Alzheimer’s disease.

In other words, sleeping pills may help some people close their eyes, but using them as a preventative treatment to ward off Alzheimer’s disease is still a fuzzy prospect that hinges on a now flimsy assumption of Alzheimer’s pathology.

That said, there is growing evidence linking sleep disturbances to Alzheimer’s disease, a disease for which there is no cure. Lucey says improving sleep hygiene and seeking treatment for sleep problems such as sleep apnea are two sensible approaches to improving overall brain health at any age.

“I hope we will eventually develop drugs that take advantage of the link between sleep and Alzheimer’s disease to prevent cognitive decline,” says Lucey. But he admits: “We’re not there yet.”

The study was published in Annals of Neurology.

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