This is the first report to delineate a pathophysiological role of the anomalous MAO-A activity upregulated by chronic intermittent hypoxia in oxidative stress and inflammation, which significantly activates the IDO-1 activity and contributes to serotonin deficiency and neurodegeneration closely associated with the clinical manifestation of the brain of patients with depression. This evidence concerns the gene IDO1 and depressive symptom measurement.