Fig. 1

Inflammation and cognitive deficits in OSAS. This figure demonstrates the important role played by inflammation in OSAS related cognitive dysfunction. CIH characterized in OSAS leads to peripheral inflammation which access the CNS through BBB or via the stimulation of vagal afferents. The high level of inflammation in the CNS further upregulates glial cells (microglia and astrocyte) activity, inducing and aggravating the neuroinflammatory reaction. Meanwhile, CIH could directly activate microglia and astrocyte, prompting the release of inflammatory cytokines in the CNS. The excessive neuroinflammatory response could in turn boost the activation of glial cells, lead to synaptic damage and losses, neuronal necrosis and apoptosis, and ultimately result in exaggerated neurocognitive deficits. In addition, treatment with CPAP, surgery, and administration of GTPs, BBG, LBPs, telmisartan, atorvastatin, NSAIDs, dexmedetomidine, and modafinil would alleviate the neuroinflammation and improve cognitive function. CIH chronic intermittent hypoxia, CNS central nervous system, BBB blood-brain barrier, CPAP continuous positive airway pressure, GTPs green tea catechin polyphenols, BBG Brilliant Blue G, LBPs Lycium barbarum polysaccharides, IL interleukin, TNF-α tumor necrosis factor-α, NF-κB nuclear factor kappa B, COX-2 cyclooxygenase-2, NSAIDs non-steroidal anti-inflammatory drugs