Common insomnia drug may help reduce Alzheimer’s-related proteins, study suggests

By Dr(h) Avi Verma

In the ongoing battle to understand and combat Alzheimer’s disease, researchers have long suspected a connection between poor sleep and the progression of the condition. A recent study offers new insight into this link, suggesting that a commonly prescribed sleeping pill may reduce the accumulation of harmful proteins associated with Alzheimer’s.

Conducted by scientists at Washington University in St. Louis, the study focused on suvorexant, a medication used to treat insomnia. The researchers discovered that taking suvorexant for two consecutive nights led to a modest decrease in two proteins, amyloid-beta and tau, which are known to accumulate in the brains of Alzheimer’s patients.

Though this study was small—limited to 38 healthy middle-aged adults with no cognitive impairments—it offers a glimpse into how promoting better sleep might help combat the early stages of Alzheimer’s disease. Sleep disturbances are often one of the first indicators of the disease, appearing long before symptoms like memory loss and cognitive decline.

The buildup of amyloid-beta can begin years before noticeable symptoms of Alzheimer’s
appear, forming plaques that interfere with brain function. Researchers believe that during deep sleep, the brain clears out these harmful proteins, and that enhancing this natural cleansing process could be a strategy for delaying or preventing Alzheimer’s.

However, the study’s lead researcher, Dr. Brendan Lucey from Washington University’s Sleep Medicine Center, urges caution. “While the findings are promising, it’s too early for those concerned about Alzheimer’s to start taking suvorexant regularly,” Lucey noted.

The research spanned just two nights and involved participants between the ages of 45 and 65, all of whom were healthy sleepers. Participants were given either a dose of suvorexant or a placebo, and samples of their cerebrospinal fluid (CSF)—the fluid surrounding the brain and spinal cord—were collected over a 36-hour period to monitor protein levels.

Even though there were no significant differences in sleep quality between the groups, those who took suvorexant showed a 10-20% reduction in amyloid-beta levels compared to the placebo group. Additionally, a higher dose of the medication temporarily reduced levels of hyperphosphorylated tau, a modified protein that plays a role in the development of tau tangles, another hallmark of Alzheimer’s.

Still, the reduction in tau levels was short-lived, with concentrations returning to normal within 24 hours after taking the medication. This indicates that while sleep aids like suvorexant may influence Alzheimer’s-related proteins, the effects are temporary and require further investigation.

The study adds to a growing body of evidence that suggests improving sleep may be key in the fight against Alzheimer’s, but long-term effects and potential risks of using sleep medications need to be thoroughly examined. Prolonged use of sleeping pills can lead to dependence and may disrupt the deeper stages of sleep that are crucial for brain health.

Dr. Lucey remains optimistic about future research, especially in older adults over a longer period of time, which could provide more definitive answers on whether sleep medications can have lasting impacts on Alzheimer’s prevention. However, he stresses that improving sleep hygiene and treating sleep disorders like sleep apnea remain critical for maintaining overall brain health.

While much is still unknown about what exactly drives Alzheimer’s disease, this study offers a hopeful step forward in understanding how sleep could play a crucial role in slowing its progression.

The findings were published in a peer-reviewed journal.