Study Objectives: This study aims to evaluate the extent to which sleep quality impacts amnestic mild cognitive impairment (aMCI)-related brain regions in a cognitively normal cohort of individuals. Methods: Seventy-four participants were rigorously evaluated using a battery of cognitive tests and a detailed clinical assessment to verify normal cognitive status. We then screened for sleep quality using the Pittsburgh Sleep Quality Index (PSQI) and depressive symptoms using the Geriatric Depression Scale (GDS). Five subjects were excluded due to mild depression. Overall 38 individuals with mean age 70.7 ± 7 were classified as poor sleepers and 31 with mean age of 69.6 ± 6 years as normal sleepers. Structural MRI and Freesurfer brain parcellation were used to measure aMCI-related brain regions. Results: Relative to normal sleepers, poor sleepers exhibited significant reductions in cortical and subcortical volumes bilaterally in the hippocampi, as well as in the superior parietal lobules and left amygdala. The effects were strongest in the left superior parietal lobule (p < .015), followed by the hippocampi. Diffuse patterns of cortical thinning were observed in the frontal lobes, but significant effects were concentrated in the right mesial frontal cortex. Lower sleep duration was most correlated with cortical volume and thickness reductions among all subjects. Conclusions: Atrophy related to poor sleep quality impacted a number of regions implicated in aMCI and Alzheimer's disease (AD). As such, interventions targeted towards improving sleep quality amongst the elderly may prove an effective tool for modulating the course of aMCI and AD.

Sleep is essential in learning and memory (Maquet, 2001).Decline in memory performance have been widely reported in patients with sleep disorders, such as insomnia and obstructive sleep apnoea (OSA) (Fortier-Brochu & Morin, 2014; Krysta, Bratek, Zawada, &Stepanczak, 2017), and in healthy population with poor or insufficient sleep (Waters & Bucks, 2011;Van Der Werf et al., 2009). The hippocampus plays a central role in regulating learning, and in memory encoding, consolidation and retrieval (Squire, 1992).A growing number of studies have investigated the relationship between sleep disorders and hippocampal volumes across the adult

We aim to determine the sleep correlates of age-related brain loss in a sample of middle-aged to older males with obstructive sleep apnea (OSA). We recruited consecutive treatment naïve male patients with moderate to severe OSA from January to November of 2019. We excluded participants if they had dementia, stroke or heart disease. We collected demographic variables and vascular risk factors. We also obtained the insomnia severity index, the Epworth sleepiness scale and the Pittsburgh sleep quality index. We also obtained computerized neurocognitive testing with the go-no-go response inhibition test, Stroop interference test, catch game test, staged information processing speed test, verbal memory test and non-verbal memory test. We derived age and education adjusted domain-specific Z-scores for global cognition, memory, attention, processing speed and executive function. We used brain MRI T1-weighted images to derive total hippocampal and gray matter volumes. Partial correlations evaluated associations between variables from sleep questionnaires (e.g., insomnia severity index score), and polysomnographic variables (the apnea-hypopnea index, average oxygen levels during sleep) with cognitive domains and brain volumes. We examined 16 participants with an age range of 40–76 years, 73% Hispanic/Latino. The mean apnea-hypopnea index was 48.9 ± 25.5 and average oxygen saturation during sleep was 91.4% ± 6.9%. Hypertension was seen in 66% and diabetes mellitus in 27%. We found that the insomnia severity index score and average oxygen levels during sleep had the strongest correlations with brain volumes and cognition. These preliminary findings may aid in developing future strategies to improve age-related brain loss in patients with OSA.

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Introduction We aim to determine the cognitive domains associated with obstructive sleep apnea (OSA) age-related brain atrophy in a sample of middle-aged to older males. Methods We evaluated consecutive treatment naïve male OSA patients (AHI≥15) without dementia, stroke or heart disease (infarction, heart failure), from March to November of 2019. We obtained demographic variables, vascular risk factors, the Epworth sleepiness scale (ESS) and the Pittsburgh sleep quality index (PSQI). We also obtained computerized neurocognitive testing with the Go-NoGo Response Inhibition Test, Stroop Interference Test, Catch Game Test, Staged Information Processing Speed Test, Verbal Memory Test and Non-Verbal Memory Test. We derived domain-specific Z-scores age and education adjusted for global cognition, memory, attention, processing speed and executive function. Pearson correlation was used to evaluate bivariate associations between the sleep exposures and neurocognitive outcomes. Linear regression was used to evaluate associations between AHI and neurocognitive domains, adjusting for the ESS. Results A total of 15 participants 40 to 76 years of age, 73% of Hispanic/Latino background, completed neurocognitive testing. The average ESS was 8.2±6.0, PSQI=5.7±4.9, and AHI=48.9±25.5. Hypertension was seen in 66% and diabetes in 27%. The AHI was correlated with global cognition (r= -0.66; p=0.008), memory (r= -0.73; p=0.002) and attention (r= -0.67; p =0.007), but not executive function or processing speed. In addition, the AHI correlated with verbal memory (r= -0.76; p=0.001), but not with non-verbal memory. In adjusted models, the AHI was associated with global cognition (β= -0.60; p=0.05) and decreased memory (β= -0.85; p=0.006). However, the association with attention was explained by the ESS. The PSQI was not correlate with the cognitive domains. Conclusion In this pilot-study, the AHI was associated with decreased global cognition, and verbal memory accounting for sleepiness. Findings suggest the left-hippocampus as a region vulnerable to early age-related brain loss in OSA. Support Scientific Advisory Committee, Pilot grant, Miller School of Medicine; R21AG056952; R21HL140437.