Destructive Sleep Apnea Research Paper

Obstructive sleep apnea (OSA) is a primary sleep disorder caused by repeated partial or complete upper airway collapse despite an ongoing effort to breathe during sleep. It is estimated that 22 million Americans suffer from OSA, affecting 24% of men and 9% of women in the middle-aged population[1] and up to 62% of older adults aged 65 or over.[2] Epidemiological studies report that OSA patients are at a greater risk of having or developing depression[3-6] and cognitive impairment.[7] In a cross-sectional epidemiological study included 5 European countries,[4] of 18,980 subjects aged 15 to 100 years, 17.6% of subjects with OSA had major depressive disorder (DSM-IV criteria for MDD),, and 18% of subjects with MDD also had OSA. After controlling
As part of the Donepezil Treatment of Cognitive Impairment and Depression (DOTCODE) clinical trial,[37] in this pilot study, in patients who received open antidepressant treatment in the first phase of the DOTCODE study we compared the differences in performance on neuropsychological tests during the initial 16 weeks of antidepressant treatment (Phase 1) between patients with and without OSA at baseline and week 16. We also evaluated baseline differences in cerebral microvascular burden and explored the regions of interest (ROIs) predicting increased risk of Alzheimer’s disease in MCI (e.g., hippocampal and entorhinal cortex volumes) between patients with and without OSA. The purpose of this study was to evaluate the impact of OSA on cognitive functions and the relationship between cognitive deficits and the changes in brain morphology in DEP-CI patients. We hypothesized (1) patients with OSA would have poorer neurocognitive performance than those with no OSA, and (2) patients with OSA would have more severe cerebral white matter damage and gray matter loss than those with no