Abstract

It is established that multiple molecules that modulate inflammation serve to regulate sleep and electroencephalogram (EEG) power spectra. The most thoroughly tested inflammatory molecules affecting sleep are the proinflammatory molecules interleukin (IL)-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α). These molecules and their receptors are involved in priming nucleotide-binding oligomerization domain-like receptor protein-3 (NLRP3) inflammasomes, which are activated by molecules involved in metabolism to activate the somnogenic molecules IL-1β and IL-18 into their mature forms. Interestingly, proinflammatory molecules tend to exhibit vasodilative properties. Growing evidence indicates that vasohemodynamics and alterations in cerebral blood flow are correlated with alterations in the EEG. Proinflammatory molecules such as IL-1β and TNF-α are produced by neurons, glia, and additional cell types that surround the vasculature in the neurovascular unit. Herein, we describe the role of neuroinflammation in the regulation of sleep and EEG power spectra including conditions with profound sleep disturbances such as autoimmune conditions and traumatic brain injury.

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