Reply to Kawada: Obstructive Sleep Apnea and Cognitive Decline in Older Adults.
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ABSTRACT:
SUBMITTER: Baril AA
PROVIDER: S-EPMC6515864 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description: Not available
| S-EPMC6515876 | biostudies-literature
Project description: Not available
| S-EPMC6943882 | biostudies-literature
Project description:Hypertension and dementia are highly prevalent in the general population. Hypertension has been shown to be a risk factor for Alzheimer's dementia and vascular dementia. Sleep apnea, another common disorder, is strongly associated with hypertension and recent evidence suggests that it may also be linked with cognitive decline and dementia. It is possible that sleep apnea is the final common pathway linking hypertension to the development of dementia. This hypothesis merits further exploration as sleep apnea is readily treatable and such therapy could foreseeably delay or prevent the onset of dementia. At present, there is a paucity of therapeutic modalities that can prevent or arrest cognitive decline. In this review, we describe the associations between hypertension, dementia and sleep apnea, the pathophysiologic mechanisms underlying these associations, and the literature examining the impact of treatment of hypertension and sleep apnea on cognition. Potential areas of future investigation that may help advance our understanding of the magnitude and direction of the interaction between these conditions and the effects of treatment of high blood pressure and sleep apnea on cognition are highlighted.
| S-EPMC6636426 | biostudies-literature
Project description:Current evidence suggests that the pathological mechanisms underlying obstructive sleep apnea (OSA) are altered with age. However, previous studies examining individual physiological traits known to contribute to OSA pathogenesis have been assessed in isolation, primarily in healthy individuals.We assessed the four physiological traits responsible for OSA in a group of young and old patients with OSA.Sleep research laboratory.Ten young (20-40 y) and old (60 y and older) patients with OSA matched by body mass index and sex.Pharyngeal anatomy/collapsibility, loop gain (LG), upper airway muscle responsiveness/gain (UAG) and the respiratory arousal threshold were determined using multiple 2- to 3-min decreases or drops in continuous positive airway pressure (CPAP). Passive pharyngeal anatomy/collapsibility was quantified as the ventilation at CPAP = 0 cmH2O immediately after the CPAP drop. LG was defined as the ratio of the ventilatory overshoot to the preceding reduction in ventilation. UAG was taken as the ratio of the increase in ventilation to the increase in ventilatory drive across the pressure drop. Arousal threshold was estimated as the ventilatory drive that caused arousal. Veupnea was quantified as the mean ventilation prior to the pressure drop. In comparison with younger patients with OSA, older patients had a more collapsible airway (ventilation at 0 cmH2O = 3.4 ± 0.9 versus 1.5 ± 0.7 L/min; P = 0.05) but lower Veupnea (8.2 ± 0.5 versus 6.1 ± 0.4 L/min; P < 0.01) and a lower LG (5.0 ± 0.7 versus 2.9 ± 0.5; P < 0.05). The remaining traits were similar between groups.Our data suggest that airway anatomy/collapsibility plays a relatively greater pathogenic role in older adults, whereas a sensitive ventilatory control system is a more prominent trait in younger adults with obstructive sleep apnea.Edwards BA, Wellman A, Sands SA, Owens RL, Eckert DJ, White DP, Malhotra A. Obstructive sleep apnea in older adults is a distinctly different physiological phenotype.
| S-EPMC4098808 | biostudies-other
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-M-NM-:B pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder. Total RNA from visceral fat of 18 subjects (10 OSA, 8 Control) was hybridized to 18 Affymetrix Genechip Human Gene 1.0 ST microarrays.
2012-09-01 | E-GEOD-38792 | biostudies-arrayexpress
Project description:Study objectivesProspective data evaluating abnormal sleep quality and quantity with cognitive decline are limited because most studies used subjective data and/or had short follow-up. We hypothesized that, over 15 y of follow-up, participants with objectively measured obstructive sleep apnea (OSA) and other indices of poor sleep quantity and quality would experience greater decline in cognitive functioning than participants with normal sleep patterns.MethodsARIC participants (n = 966; mean age 61 y, 55% women) with in-home polysomnography (1996-1998) and repeated cognitive testing were followed for 15 y. Three cognitive tests (Delayed Word Recall, Word Fluency, and Digit Symbol Substitution) were administered at two time points (1996-1998 and 2011-2013). Ten additional cognitive tests were administered at the 2011-2013 neurocognitive examination. OSA was modeled using established clinical OSA severity categories. Multivariable linear regression was used to explore associations of OSA and other sleep indices with change in cognitive tests between the two assessments.ResultsA median of 14.9 y (max: 17.3) passed between the two cognitive assessments. OSA category and additional indices of sleep (other measures of hypoxemia and disordered breathing, sleep fragmentation, sleep duration) were not associated with change in any cognitive test. Analyses of OSA severity categories and 10 cognitive tests administered only in 2011-2013 also showed little evidence of an association.ConclusionsOverall, abnormal sleep quality and quantity at midlife was not related to cognitive decline and later-life cognition. The effect of adverse sleep quality and quantity on cognitive decline among the elderly remains to be determined.
| S-EPMC4712410 | biostudies-literature
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-κB pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder.
2012-09-01 | GSE38792 | GEO
Project description: Not available
| S-EPMC7258636 | biostudies-literature
Project description:Research reveals mixed evidence for the effects of adenotonsillectomy (AT) on cognitive tests in children with obstructive sleep apnea syndrome (OSAS). The primary aim of the study was to investigate effects of AT on cognitive test scores in the randomized Childhood Adenotonsillectomy Trial. Children ages 5 to 9 years with OSAS without prolonged oxyhemoglobin desaturation were randomly assigned to watchful waiting with supportive care (n = 227) or early AT (eAT, n = 226). Neuropsychological tests were administered before the intervention and 7 months after the intervention. Mixed model analysis compared the groups on changes in test scores across follow-up, and regression analysis examined associations of these changes in the eAT group with changes in sleep measures. Mean test scores were within the average range for both groups. Scores improved significantly (P < .05) more across follow-up for the eAT group than for the watchful waiting group. These differences were found only on measures of nonverbal reasoning, fine motor skills, and selective attention and had small effects sizes (Cohen's d, 0.20-0.24). As additional evidence for AT-related effects on scores, gains in test scores for the eAT group were associated with improvements in sleep measures. Small and selective effects of AT were observed on cognitive tests in children with OSAS without prolonged desaturation. Relative to evidence from Childhood Adenotonsillectomy Trial for larger effects of surgery on sleep, behavior, and quality of life, AT may have limited benefits in reversing any cognitive effects of OSAS, or these benefits may require more extended follow-up to become manifest.
| S-EPMC4960728 | biostudies-literature
Project description:Sleep laboratory studies find that restricted sleep duration leads to worse short-term cognition, especially memory. Observational studies find associations between self-reported sleep duration or quality and cognitive function. However self-reported sleep characteristics might not be highly accurate, and misreporting could relate to cognition. In the Sleep Study of the National Social Life, Health, and Aging Project (NSHAP), a nationally representative cohort of older US adults (2010-2015), we examined whether self-reported and actigraph-measured sleep are associated with cross-sectional cognitive function and 5-year cognitive decline. Cognition was measured with the survey adaptation of the multidimensional Montreal Cognitive Assessment (MoCA-SA). At baseline (n = 759), average MoCA-SA score was 14.1 (standard deviation, 3.6) points of a possible 20. In cross-sectional models, actigraphic sleep-disruption measures (wake after sleep onset, fragmentation, percentage sleep, and wake bouts) were associated with worse cognition. Sleep disruption measures were standardized, and estimates of association were similar (range, -0.37 to -0.59 MoCA-SA point per standard deviation of disruption). Actigraphic sleep-disruption measures were also associated with odds of 5-year cognitive decline (4 or more points), with wake after sleep onset having the strongest association (odds ratio = 1.43, 95% confidence interval: 1.04, 1.98). Longitudinal associations were generally stronger for men than for women. Self-reported sleep showed little association with cognitive function.
| S-EPMC6545284 | biostudies-literature