Among older adults with severe obstructive sleep apnea (OSA), less slow-wave sleep (SWS) is associated with more white matter (WM) abnormalities, according to study findings published in Neurology.
The burden of WM hyperintensities (WMH) has been associated with risk for mild cognitive impairment, dementia, and stroke. As such, WM abnormalities are a subset of vascular contributions to cognitive impairment and dementia (VCID). To date, there are no treatments for VCID other than risk factor management.
For the study, researchers evaluated whether SWS may be a risk factor for WM abnormalities. The researchers sourced data for this study from the Mayo Clinic Study of Aging (MCSA), which was a large, population-based cohort study of community-dwelling adults who were recruited starting in 2004. Individuals (N=140) with OSA who were free from dementia and had undergone magnetic resonance imaging (MRI) and polysomnography (PSG) were evaluated for the relationship between SWS and WM abnormalities.
The participants were mean age, 72.7 (SD, 9.6) years; 60% were men; and, 90.7% were deemed cognitively unimpaired in both MRI and PSG evaluations. During MRI, 140 participants exhibited WMH and 103 fractional anisotropy (FA) of the genu of the corpus collosum (genu FA).
In the fully adjusted models, every 10-point decrease in the proportion of time spent in the nonrandom eye movement sleep stage 3 (N3%) associated with a 0.058 (95% CI, 0.006-0.111; P =.030) increase in the log of WMH, which was a similar effect as that of aging 2.3 years. This effect was more pronounced among only individuals older than 60 years (n=121), in which a 10-point decrease in N3% resulted in a 0.075 (95% CI, 0.018-0.132; P =.011) increase in the log of WMH.
Similarly, every 10-point decrease in N3% associated with a 0.006 (95% CI, -0.012 to -0.0002; P =.042) decrease in the log of genu FA, which was similar to aging 3 years. After removing individuals who did not reach N3 sleep, the remaining participants (n=81) had an even more pronounced relationship between N3% and genu FA (b, 0.009; 95% CI, 0.0017-0.016; P =.016).
In a post hoc analysis, pairs of individuals with mild or moderate (n=42) and severe (n=42) OSA were matched. Among this matched cohort, those with severe OSA had higher WMH (median, 0.007 vs 0.006; P =.042) and reduced genu FA (median, 0.57 vs 0.63; P =.007), compared with mild or moderate OSA, respectively.
These findings may have been biased, as PSG data were collected during an in-lab split-night PSG study, which may not be indicative of real-world sleep.
The researchers noted, “[R]educed SWS and higher OSA burden are independently associated with cerebrovascular biomarkers in predominantly cognitively unimpaired older adults, which can contribute to greater risk of MCI, dementia, and stroke.” “Further longitudinal studies will be required to assess the directionality of these associations and the trajectory of [cerebrovascular disease] biomarkers in relationship to OSA treatment and/or strategies to improve sleep quality or even enhance SWS,” they concluded.
Disclosures: Some study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures.
Carvalho DZ, McCarter SJ, St Louis EK, et al. Association of polysomnographic sleep parameters with neuroimaging biomarkers of cerebrovascular disease in older adults with sleep apnea. Neurology. Published online May 10, 2023. doi:10.1212/WNL.0000000000207392