Research is shedding light on the connection between poor sleep and Alzheimer's disease. A recent study by Washington University in St. Louis examined the impact of the insomnia medication Suvorexant on the build-up of toxic proteins associated with Alzheimer's disease. The study involved 38 healthy adults with no cognitive impairment or sleep issues.
The researchers found that taking suvorexant for just two nights slightly reduced the levels of two key proteins linked to Alzheimer's disease: amyloid-beta and tau. These proteins accumulate in the brain and are associated with forming plaques and tangles, contributing to cognitive decline.
Sleep disturbances, such as insomnia, can be early warning signs of Alzheimer's disease before memory loss and cognitive decline. The study suggests improving sleep quality could help the brain clear out these harmful proteins and waste products.
However, the researchers caution against interpreting these findings as a reason to start taking Suvorexant regularly. The study was short-term and involved healthy individuals, not those with sleep disorders or cognitive impairment.
Interestingly, previous research by the same team had shown a link between poor-quality, shallow sleep elevated tau levels and amyloid-beta proteins. This raises concerns about the effectiveness of sleeping pills in promoting deep, restorative sleep.
In the study, participants received either a Suvorexant or a placebo, and their cerebrospinal fluid was sampled to measure protein levels. The results showed that amyloid-beta concentrations decreased by 10 to 20 per cent using suvorexant, and a higher dose temporarily reduced levels of hyperphosphorylated tau, a modified form of tau protein linked to tangle formation and cell death. However, these effects were not long-lasting.
While the study suggests a potential link between improved sleep and reduced protein levels associated with Alzheimer's, it is important to note that the underlying causes of Alzheimer's disease are still not fully understood. The prevailing theory that abnormal protein clumps drive the disease has faced challenges, as efforts to lower amyloid levels have not yet yielded effective treatments.