Sleep deprivation in healthy people leads to the accumulation of a protein fragment associated with abnormalities in brain function and Alzheimer’s disease.
The study, “β-Amyloid accumulation in the human brain after one night of sleep deprivation,” published in the Proceedings of the National Academy of Sciences of the United States of America, assessed the effect of one-night sleep deprivation on the accumulation of β-amyloid in the brains of a group of healthy participants.
One of the hallmarks of Alzheimer’s disease is the formation of protein plaques and tangles between nerve cells. These are made of so-called beta-amyloid fragments that stick together and accumulate between nerve cells, disrupting their function.
Previous research in animal models has shown that sleep restriction can lead to the build-up of beta-amyloid in animals’ brains. However, not much is known about the impact of sleep deprivation on β-amyloid burden in the human brain.
The study involved 20 healthy individuals whose 22 to 72 years old (average 39.8 years). There was an equal number of women and men.
Beta-amyloid levels were measured using a specific radioactive material that can the be quantified using an imaging technique known as positron emission tomography (PET). These measurements were performed after the individuals had a night of restful sleep (referred to as rested-wakefulness) and after the individuals had a one-night sleep deprivation (approximately 31 hours without sleep).
The results showed that after sleep deprivation, there was a significant increase in the levels of beta-amyloid compared to after a state of rested-wakefulness. Furthermore, beta-amyloid accumulation following sleep deprivation was more noticeable in brain areas known to be involved in the pathology of Alzheimer’s, namely, the hippocampus and thalamus.
The authors concluded that in the individuals tested the “study documents an effect of one-night [sleep deprivation] on [Aβ] in the hippocampus, thus providing preliminary evidence that sleep, among other factors, could influence Aβ clearance in the human brain.”
It is important to note, however, that the number of participants was very small and, as such, no generalization to the population can be made solely based on this study.