Common Sleep Medication May Reduce Alzheimer’s-Related Protein Build-Up, Study Finds

There is still much to uncover about Alzheimer’s disease, but researchers are actively investigating the connection between disturbed sleep and the progression of the condition.

In a recent study published earlier this year, scientists discovered that the use of sleep aids to improve sleep quality could potentially decrease the accumulation of harmful protein clusters in the cerebrospinal fluid, which serves as the brain’s nightly cleaning system.

Scientists from Washington University in St. Louis discovered that individuals who received suvorexant, a common remedy for insomnia, for two consecutive nights at a sleep clinic showed a modest reduction in the levels of two proteins, amyloid-beta and tau, which are known to accumulate in Alzheimer’s disease.

Significance of a Short Study with a Small Group in Illuminating the Link Between Sleep and Alzheimer’s Molecular Markers

While this study was relatively short and involved a small cohort of healthy adults, it serves as a noteworthy demonstration of the connection between sleep and the molecular indicators of Alzheimer’s disease.

Sleep disturbances can serve as an early indicator of Alzheimer’s, often preceding other symptoms like memory loss and cognitive decline. By the time these initial symptoms manifest, abnormal amyloid-beta levels are typically at their peak, forming clumps known as plaques that obstruct brain cell function.

Researchers believe that promoting better sleep might be one approach to delay the onset of Alzheimer’s disease by enabling the brain to clear out accumulated proteins and waste products from the day.

Caution from Neurologist Brendan Lucey

However, neurologist Brendan Lucey, who led the study at Washington University’s Sleep Medicine Center, cautioned that it would be premature for individuals concerned about Alzheimer’s to interpret these findings as a reason to start using suvorexant on a nightly basis.

The research was limited to a brief duration of two nights and encompassed 38 middle-aged participants who displayed no cognitive impairments and had no existing sleep-related issues.

Relying on sleeping pills over an extended period is not an advisable solution for individuals experiencing sleep deficits, as it can lead to dependence.

Moreover, sleeping medications might induce lighter sleep phases rather than deep, restorative slumber. This could pose a challenge since earlier studies conducted by Lucey and his team uncovered a correlation between lower-quality slow-wave sleep and elevated levels of tau tangles and amyloid-beta proteins.

Investigating the Impact of Sleeping Pills on Cerebrospinal Fluid Levels of Tau and Amyloid-Beta

In their most recent investigation, Lucey and colleagues aimed to determine if enhancing sleep with the assistance of sleeping pills could result in reduced levels of tau and amyloid-beta in the cerebrospinal fluid that surrounds the brain and spinal cord. Previous research has demonstrated that even a single night of disrupted sleep can cause a surge in amyloid-beta levels.

A group of volunteers aged between 45 and 65 years old received one of two doses of suvorexant or a placebo pill. An hour after this administration, researchers collected a small sample of their cerebrospinal fluid.

Over the course of 36 hours, while the participants slept and throughout the following day and night, the researchers continued to collect samples every two hours to monitor changes in protein levels.

Amyloid-Beta Levels Reduced by Suvorexant Despite Comparable Sleep Quality Among Groups

Interestingly, despite no differences in sleep quality observed between the groups, individuals who received a typical insomnia-prescribed dose of suvorexant experienced a reduction in amyloid-beta concentrations ranging from 10% to 20%, in comparison to those who received a placebo.

The higher suvorexant dosage also momentarily lowered levels of hyperphosphorylated tau, which is a modified form of the tau protein associated with the formation of tau tangles and neuronal cell death.

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

Neurologist Brendan Lucey expressed optimism, suggesting that if tau phosphorylation can be reduced, it might lead to a decrease in tangle formation and neuronal cell death. He remains hopeful that future studies involving older adults taking sleeping pills for extended periods could potentially measure a sustained impact on protein levels, while acknowledging the need to carefully assess any potential drawbacks of using sleeping medications.

Naturally, all of this hinges on our comprehension of the underlying causes of Alzheimer’s disease.

Rethinking Alzheimer’s Pathology

The dominant theory, which suggests that abnormal protein aggregates play a pivotal role in driving Alzheimer’s pathology, has recently faced significant scrutiny. Despite decades of research dedicated to reducing amyloid levels, no practical drugs or therapies have emerged to effectively prevent or slow down the disease. Consequently, researchers have been compelled to reevaluate their understanding of how Alzheimer’s disease actually develops.

In simpler terms, while sleeping pills may assist some individuals in achieving better sleep, utilizing them as a preventative measure against Alzheimer’s disease remains uncertain, particularly given the current uncertainties surrounding the Alzheimer’s disease hypothesis.

Nonetheless, there is growing evidence linking sleep disturbances to Alzheimer’s disease, a condition for which effective treatments remain elusive. Brendan Lucey suggests that improving sleep habits and seeking treatment for sleep-related issues like sleep apnea represent reasonable strategies for enhancing overall brain health, regardless of age.

“I’m optimistic that we will eventually develop medications that leverage the connection between sleep and Alzheimer’s to prevent cognitive decline,” Lucey remarked. However, he acknowledged, “We haven’t reached that point just yet.”

Read the original article: Science Alert

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