Sleep and Neuroinflammation

The intricate interplay between sleep regulation and neuroinflammation involves a symbiotic relationship, with immune-related molecules taking centre stage in this dynamic interaction. Beyond their conventional immune functions, cytokines and immune signalling components emerge as pivotal determinants of sleep patterns. Notably, interleukin-1 beta (IL-1β) and tumour necrosis factor-alpha (TNF-α), both pro-inflammatory cytokines, wield considerable influence over sleep modulation, encompassing key aspects such as slow-wave activity and non-rapid eye movement (NREM) sleep. A compelling facet of these cytokines is their adherence to a daily oscillation, hinting at intricate temporal entanglements with the sleep process. Recent inquiries into the NLRP3 inflammasome, recognized for its role in cytokine processing and secretion, unveil fresh perspectives on sleep regulation. By impacting the production of IL-1β, the NLRP3 inflammasome, activated by diverse cellular stressors, substantially shapes sleep architecture. Other inflammatory molecules such as adenosine, ATP, chemokines, neurotrophins, and reactive oxygen species give an insight into the complex interplay between sleep-modulating processes. Continued exploration of the complex interplay between these fundamental processes offers a more comprehensive understanding of their underlying mechanisms. This, in turn, opens possibilities for interventions to refine sleep quality and address associated sleep disorders.