A recent breakthrough in Alzheimer’s prevention may come from an unexpected source—a medication typically used to combat insomnia.
Suvorexant, widely prescribed for sleep-related issues, is now under investigation for its capacity to impede the development of hallmarks in Alzheimer’s. Researchers at Washington University in St. Louis have uncovered that administeration of this sleep aid over a short term led to a modest reduction of amyloid-beta and tau proteins in the brain, elements closely linked with Alzheimer’s formation.
Delving into the relationship between sleep disturbances and the early stages of Alzheimer’s.
Neurologist Brendan Lucey and his team pursued a novel approach. Sleep complications can forewarn the prospect of Alzheimer’s, often appearing before conventional manifestations of the disease. When such early signs emerge, amyloid-beta levels could be nearing a critical threshold, Lucey notes, making it imperative to explore early intervention strategies.
The link between sustenance of healthy brain function and quality sleep was at the forefront of this study.
It encompassed a small group of 38 participants, all middle-aged and not showing signs of either cognitive decline or irregularities in sleep patterns. These individuals were subject to a regimen that involved either suvorexant or a placebo, following which cerebrospinal fluid samples were gathered over a 36-hour timeline. These samples provided insight into the medication’s impact on protein levels during and after the sleep cycle.
Findings from this inquiry revealed that a standard dose of suvorexant corresponded with a reduction in amyloid-beta levels.
They experienced a decrease of about 10 to 20 percent when compared to the placebo. Furthemore, an elevated dose seemed to momentarily reduce hyperphosphorylated tau—a more harmful tau protein variation known for fuelling tangle formations and cellular death. Lucey sees potential in this outcome, suggesting that hindering tau phosphorylation could crucially diminish such detrimental processes over the long term.
Yet, despite these initial positive results, Lucey advises a cautious perspective.
Before advocating for the regular use of suvorexant for Alzheimer’s prevention, one must consider several factors. The study canvassed only a brief snapshot in time, and the drawbacks of sleeping pill usage, including dependency risks and the triggering of inadequate sleep cycles, need thorough consideration. Furthermore, former research has stressed that the most restorative sleep phase—deep sleep—is essential for minimizing tau tangles and amyloid-beta clusters.
Lucey supports circumspect, non-pharmacological methods like refining sleep hygiene and professionally addressing sleep disturbances to enhance cerebral well-being.
He maintains hope for future pharmaceutical advancements that exploit the sleep-Alzheimer’s nexus to stave off cognitive deterioration, stating, “We’re not there yet.”
These investigative results are documented in the Annals of Neurology, reflecting the confluence of sleep irregularities and Alzheimer’s, a disease for which substantial remedies continue to be elusive..