# Sleep macro‐architecture, nocturnal hypoxemia, and Alzheimer's Disease‐related MRI patterns among diverse older adults

## TL;DR

This study finds that poor sleep patterns and low nighttime oxygen levels are linked to brain changes associated with Alzheimer's disease in a diverse group of older adults.

## Contribution

The study provides novel evidence on how sleep macro-architecture and hypoxemia relate to Alzheimer's-related MRI patterns across ethnoracial groups.

## Key findings

- Higher light sleep and longer REM latency are linked to thinner cortex in Alzheimer's-related brain regions.
- Lower deep sleep and REM sleep apnea are associated with increased white matter hyperintensities.
- Nocturnal hypoxemia is independently linked to greater white matter hyperintensity volume.

## Abstract

Increasing evidence has linked sleep quality and sleep apnea to poorer brain health, yet the association between sleep macro‐architecture, nocturnal hypoxemia and Alzheimer's Disease (AD)‐related patterns on neuroimaging remains less known, especially across older adults from diverse ethnoracial groups.

The recently completed Health and Aging Brain Study‐Health Disparities (HABS‐HD)‐Dormir Study recruited community‐dwelling non‐Hispanic White (NHW), Hispanic, and Black participants who underwent an in‐home sleep apnea assessment (WatchPAT, Itamar, IS) and brain magnetic resonance imaging (MRI) to evaluate sleep and AD‐related MRI biomarkers. Sleep stages were estimated using a validated proprietary algorithm. Our primary outcomes are AD‐signature cortical thickness (in individual regions of interests, including entorhinal cortex, fusiform gyrus, inferior temporal gyrus, and middle temporal gyrus, N = 636) and white matter hyperintensities (WMH) volume [log(WMH+1), normalized by intracranial volume, and categorized into tertiles, N = 842]. We applied multivariable linear or ordinal regression models adjusting for age, sex, ethnicity, education, body mass index, cognitive status, smoking, alcohol consumption, and MRI scanner.

A total of 842 elderly participants [34% male; 42% NHW, 33% Hispanic and 25% Black; age 66.18.6 years] were included in the final analysis. Greater light sleep percentage and longer REM sleep latency were independently associated with thinner cortex in AD‐signature regions: standardized β
light sleep percentage per 1‐SD increase = ‐0.12 [95% confidence interval (95%CI), ‐0.19 to ‐0.05, false discovery rate (FDR)‐adjusted p = 0.007], β
REM sleep latency per 1‐SD increase = ‐0.14 (95%CI, ‐0.21 to ‐0.07, p<0.001); while inverse pattern was observed for deep sleep percentage: β
deep sleep percentage per 1‐SD increase = 0.12 (95%CI, 0.05 to 0.19, p = 0.006) (Figure 1). Higher AHI in REM sleep and mean oxygen saturation<94% (the median value of study sample) were independently associated with greater WMH volume: odds ratioAHI in REM sleep per 1‐SD increase = 1.18 (95%CI, 1.02 to 1.36, p = 0.048), odds ratiomean oxygen saturation<94% per 1‐SD increase = 1.38 (95%CI, 1.04 to 1.83, p = 0.049) (Figure 2). There were no ethnoracial interactions for these associations.

Light/deep sleep percentage, longer REM sleep latency, and nocturnal hypoxemia were associated with AD‐related MRI patterns.