A new study has revealed a stark connection between sleep deprivation and increased deposits of amyloid-beta – peptides linked to Alzheimer's disease – in the human brain. This is the first study to clearly measure the increase in amyloid-beta in specific areas of the human brain after just one night's disturbed sleep.
The research recruited 20 healthy subjects and measured their baseline levels of amyloid-beta brain deposits using positron emission tomography (PET), with the tests repeated after the subjects had experienced one night of sleep deprivation. The results showed significantly increased levels of amyloid-beta in the brain after just one sleep deprived night, with increases particularly observed in two brain regions commonly implicated in the onset of Alzheimer's disease, the right hippocampus and thalamus.
This study, led by researchers from the National Institutes of Health in Bethesda follows on from work published earlier this year by the Washington University School of Medicine. That earlier research established a earlier research established a direct correlation between disrupted sleep and an increase in amyloid-beta brain deposits in healthy, middle-aged people.
There are significant limitations to how broadly we can interpret the results of this study. While the build-up of amyloid-beta plaques in the brain deposits is certainly one of the central pathological observations seen in people with Alzheimer's disease, it's unclear whether these acute sleep-related amyloid-beta increases actually accumulate over a long period of time and result in dementia-related conditions. The authors of this new study do point out that the act of sleep does serve to flush the brain of amyloid-beta, so it's uncertain whether these short term increases subside after a person gets a decent night's rest.
Leon Lack, a Professor from Flinders University who did not work on this new research, says that while the study is important in how it shows the effects of acute sleep deprivation on the brain, there are major questions surrounding any long term implications. Lack uses the example of an Australian sea lion to explain how an animal potentially adapts to disrupted or altered sleep patterns.
"The Australian sea lion experiences regular (about weekly) episodes of two to three days of complete sleep deprivation foraging in the sea for fish and then recovers lost sleep with three to four days of sleep and relaxation on the beach," says Lack. "We don't know for certain but it doesn't appear that they suffer any Alzheimer's disease."
Doug Brown, Chief Policy and Research Officer at Alzheimer's Society, also notes that, while this is a fascinating study, it doesn't provide any conclusive link between sleep deprivation and dementia.
"Though several studies have suggested that amyloid beta builds up when we lack sleep, and previous evidence has shown sleep may give the brain a chance to clear out clumps of amyloid beta, unfortunately none have been able to confirm that sleep deprivation can cause dementia," says Brown. "This study can't give us a definitive answer either, as it only looked at a very small number of people for a short period of time, none of whom had dementia."
Another intriguing hypothesis raised by the researchers in this new study is a connection between increased amyloid-beta brain deposits and a negative mood following sleep deprivation. The authors suggest that the hippocampus and thalamus have been shown to play a major role in irregular mood disorders, and the rise in amyloid-beta following sleep deprivation could explain these acute mood changes.
What we can be sure of at this stage is that sleep is undoubtedly an important process, and when disrupted it can result in a number of significant negative symptoms, both physically and psychologically. Good sleep is fundamental to proper brain function, but whether sleep deprivation, or disruption, plays a major role in the onset of dementia is still yet to be proven.
The new research was published in the journal PNAS.
