Blood-Brain Barrier Disruption Induced by Chronic Sleep Loss: Low-Grade Inflammation May Be the Link

Figure 1

Potential inflammatory mediators participating in the regulation of blood-brain barrier permeability during sleep loss. The figure shows the platform method to induce sleep loss in the rat. Chronic sleep restriction increases blood-brain barrier permeability to circulating molecules (e.g., Evans blue) and sleep recovery promotes restoration of normal blood-brain barrier permeability. Inflammatory mediators with barrier regulation properties, such as tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), interleukin-1β (IL-1β), and IL-17A, are released during sleep loss conditions and some of them return to basal levels during sleep recovery; others, like IL-17A and TNF-α, are maintained at high levels despite sleep recovery. The barrier changes induced by inflammatory mediators may lead to neuroinflammation and potentially may underlie the cognitive impairments induced by sleep loss.