Blood-Brain Barrier Disruption Induced by Chronic Sleep Loss: Low Grade Inflammation May Be the Link
The effects of chronic sleep loss on blood-brain barrier.
Sleep is a vital phenomenon related to immunomodulation at the central and peripheral level. Sleep deficient in duration and/or quality is a common problem in the modern society and is considered a risk factor to develop neurodegenerative diseases. Sleep loss in rodents induces blood-brain barrier disruption and the underlying mechanism is still unknown. Several reports indicate that sleep loss induces a systemic low-grade inflammation characterized by the release of several molecules, such as cytokines, chemokines, and acute-phase proteins; all of them may promote changes in cellular components of the blood-brain barrier, particularly on brain endothelial cells. In the present review we discuss the role of inflammatory mediators that increase during sleep loss and their association with general disturbances in peripheral endothelium and epithelium and how those inflammatory mediators may alter the blood-brain barrier. Finally, this manuscript proposes a hypothetical mechanism by which sleep loss may induce blood-brain barrier disruption, emphasizing the regulatory effect of inflammatory molecules on tight junction proteins.
Chronic sleep loss induces systemic low grade inflammation that may be related to epithelial and endothelial disturbances both at the systemic and at the central level. Particularly, the role of inflammatory mediators in the blood-brain barrier disruption induced by sleep loss might explain the cognitive impairment associated with sleep loss. The systemic and local effect of inflammatory molecules accumulated during chronic sleep loss should be taken into account for the study of general consequences of sleep deficiency including the risk of developing neurologic and neurodegenerative diseases.