Sleep Macroarchitecture, Obstructive Sleep Apnea Impact Global Cognition

Better sleep consolidation and the absence of obstructive sleep apnea (OSA) correlated with improved scores indicative of superior global cognitive functioning, according to study findings published in JAMA Network Open.

Researchers in Australia and the United States conducted a prospective cohort study of 5946 individuals (median age, 56-89; 31.5% women; 91.7% White; 3.9% Black) living in 5 communities participating in the Sleep and Dementia Consortium to analyze the associations of poor sleep microarchitecture and OSA with development of cognitive impairment over a 5-year period.

Comprehensive baseline overnight, home-based polysomnography (PSG) assessments were conducted between 1995 and 1998. Daytime sleepiness was measured via the Epworth Sleepiness Scale (ESS). The apnea-hypopnea index (AHI) was used to determine OSA severity.

The median wake after sleep onset time ranged from 44 minutes to 101 minutes across the 5 cohorts. The incidence of moderate-to-severe OSA ranged from 16.9% to 28.9%, whereas mild OSA ranged from 45.2% to 63.9% across the 5 cohorts.

Higher sleep maintenance efficiency (pooled β per 1% increase: 0.08; 95% CI, 0.03 to 0.14; P <.01) and lower wake after sleep onset times (pooled β per 1-minute increase: -0.07; 95% CI, -0.13 to -0.01; P =.02) correlated with better global cognition performance. This finding supports previous research suggesting that cognition may be connected to specific features of non-rapid eye movement (REM) sleep macroarchitecture.

Shorter total sleep times of 6 hours or less were associated with poorer scores for attention and processing speed (pooled β: 0.07; 95% CI, 0.02 to 0.11; P <.01). Interestingly, sleep microarchitecture did not significantly impact learning, memory, or visuospatial abilities in this study despite the recognized role of sleep in memory consolidation.

In contrast, compared with those without OSA, mild to severe OSA (pooled β: -0.06; 95% CI, -0.11 to -0.01; P =.01) correlated with poorer global cognition. Similar findings were demonstrated when analyzing moderate-to-severe OSA (pooled β: -0.06; 95% CI, -0.11 to -0.01; P =.02) compared with those without OSA.

Intermittent hypoxia leading to ischemic brain injury or sleep fragmentation and systemic inflammation or cardiovascular instability are possible theories explaining why OSA might contribute to poorer cognition, although this observational study did not assess causation.

The researchers did not observe any associations between sleep and OSA status with gender, excessive daytime sleepiness via the Epworth Sleepiness Scale (ESS) scores, and APOEe4 genotype.

“Evidence from multiple population-based cohorts indicated that better sleep consolidation and the absence of OSA were associated with superior general cognitive function,” the researchers wrote. “With respect to individual cognitive domains, only short sleep duration was associated with poorer attention and processing speed,” they explained.

The researchers strongly encouraged future research to investigate the relationship between poor sleep and cognitive impairment and dementia.

Study limitations included assessment of sleep and cognition at only 1 point in time and relatively short follow-up duration, negating the ability to assess temporal, bidirectional associations between poor sleep and cognitive impairment.

Disclosures: Several study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see original source for full list of disclosures.

This article originally appeared on Neurology Advisor