The Effects of Sleep Deprivation on the Human Brain
The Effects of Sleep Deprivation on the Human Brain
23 June 2026
The vital importance of sleep for human health is becoming increasingly well understood. David Elmenhorst, a sleep expert at the Forschungszentrum Jülich, has been conducting research on the effects of chronic sleep deprivation for many years. In his latest study on the topic, he was able to directly measure, for the first time, changes in synaptic density caused by sleep in humans. In this interview, he explains the significance of his work.
Prof. Dr. David Elmenhorst, a sleep expert at the Forschungszentrum Jülich, has been studying the effects of sleep deprivation on the human brain for many years.Copyright: Forschungszentrum Jülich / Sascha Kreklau
How did you sleep last night?
David Elmenhorst: Laughs… Good… Okay, I should go to bed earlier.
What is a good analogy for you to explain what sleep means for our brain?
DW: Sleep is the time for maintenance work that can only be carried out once normal operations have ceased: the system is cleaned up and metabolic waste is removed. Important memories are archived and unnecessary information is deleted. Neural connections are adjusted, and synapses are strengthened or broken down.
How would you describe the most important finding of your study in one sentence?
DW: Connections between our nerve cells in the brain are established and broken down in astonishing numbers every day through wakefulness and sleep.
What has previous research on this topic already shown, and what does this study add?
DW: The homeostasis hypothesis of sleep-wake regulation posits that synaptic density and strength increase during wakefulness and decrease during sleep. This has already been demonstrated in animal studies, e.g., in fruit flies or mice. Given the importance of synaptic plasticity, we have transferred these findings from animals to humans. Prolonged sleep deprivation significantly increased synaptic density, and this increase was associated with an increase in deep sleep activity during restorative sleep, suggesting a link between prolonged wakefulness, synaptic strengthening, and a subsequent sleep-dependent return to baseline levels.
We believe that our results make a valuable contribution to the field of research, particularly in elucidating the extent of daily fluctuations in synaptic density. This extent is significant for the clinical interpretation of observed differences in synaptic structures in disorders such as depression, schizophrenia, or dementia.
To our knowledge, this is the first longitudinal study in humans to directly measure changes in synaptic density caused by sleep. Our findings bridge an important gap between cell-level research and human imaging studies and may expand our understanding of the role of sleep in brain plasticity and mood regulation.
What are the methodological challenges involved in investigating the relationships between sleep deprivation and synaptic density in humans?
DW: Investigating these relationships in humans is challenging for several reasons. A central problem is that the methods previously used in animals, such as the direct removal of brain tissue, are invasive and simply cannot be applied to humans. We therefore rely on imaging techniques such as positron emission tomography, which, however, is costly and limited in its spatial resolution. Another challenge lies in clearly isolating the influence of sleep. While we can strictly control sleep, physical activity, light, diet, and social interaction in the laboratory, this is artificial and limited to short periods. What happens in the lab does not necessarily reflect everyday life. Furthermore, people differ significantly from one another in their sleep architecture, their sensitivity to sleep deprivation, and their brain structure. Therefore, it is necessary to study a group of people to make generalizable statements. And finally, to obtain meaningful results, we need repeated measurements on the same individuals over a longer period of time, which is more taxing for the participants and at the same time more methodologically complex.
You show an increase in a marker for synaptic density after sleep deprivation. What does that mean specifically?
DW: It means that at the end of the day, the brain exhibits more active synapses in several areas—that is, more connections between nerve cells are active simultaneously, suggesting that the brain continuously forms new connections while awake. What is particularly interesting is that this increase is associated with heightened deep-sleep activity during the subsequent night of rest. Nighttime sleep then helps to restore balance to the synaptic connections.
Did anything about the results particularly surprise you?
DW: What really surprised me is the extent of the changes caused by just a single night without sleep, which produces measurable differences in synaptic density across many brain regions. If sleep has such an immediate impact on the nervous system even in healthy people, what does that mean for people with depression or other mental illnesses?
Are the results of your study also helpful in this regard; could they, for example, become significant for clinical diagnostics?
DW: If we better understand how much synaptic markers fluctuate in healthy people due solely to sleep and wakefulness, we will be able to more precisely determine in the future whether changes we observe in patients with depression, schizophrenia, or dementia are actually disease-related.
