Fig. 7.

Proposed interactions between neurological disorders and other pathological processes induced by OSAS/IH-induced elevated ROS levels. OSAS/IH upregulates the expression of ROS in the brain, and the inhibitory effect of protective neurotrophic factors on ROS is weakened, which further leads to an increase in ROS. The macromolecular substances in injured nerve cells cause nerve cell death and activate inflammation-related signaling pathways to release inflammatory factors. Sympathetic nerve activation by OSAS/IH could cause cognitive impairment independently of other mechanisms. In addition, OSAS/IH can directly activate microglia and astrocytes and promote the release of inflammatory cytokines in the central nervous system. Excessive neuroinflammatory responses could, in turn, promote the activation of glial cells, resulting in synaptic damage and loss, neuronal necrosis, and apoptosis and ultimately leading to exaggerated neurocognitive dysfunction. BDNF brain-derived neurotrophic factor, Mn-SOD superoxide dismutase, CAT catalase, COX-2 cyclooxygenase-2, iNOS inducible nitric oxide synthase