Pathogenesis of Cognitive Dysfunction in Patients with Obstructive Sleep Apnea: A Hypothesis with Emphasis on the Nucleus Tractus Solitarius

Figure 1

Schematic representation of the pathogenesis of cognitive decline in patients with sleep disordered breathing. Several risk factors upregulate proinflammatory cytokines and induce systemic inflammation. The latter then promotes neuroinflammation which augments further inflammation; this has a negative impact on neuronal, glial, and vascular endothelial cell functions. Inflammation, intermittent hypoxia, and oxidative stress provide a rich milieu causing the NTS inflammation and dysfunction. Being a central hub for processing disparate afferents and owing to its widespread projections in the CNS, the dysfunctional NTS would negatively impact several key brain foci and their physiological functions. Dysfunctional NTS and hypoglossal nuclei would cause genioglossus dysfunction resulting in pharyngeal obstruction/collapse. This leads to snoring, OSA, intermittent hypoxia, and hypoxemia. Thus, neuroinflammation and sleep apnea are major contributing factors that may cause neuronal degeneration and provoke cognitive dysfunction.