Asymptomatic Sleep Disordered Breathing Could Forecast Alzheimer Disease


Better testing for SDB and other sleep disorders are needed for the older population.

Gael Chetelat, PhD

Gael Chetelat, PhD

This article, "Sleep-Disordered Breathing Linked to Alzheimer Disease Brain Changes," was originally published in NeurologyLive.

Screening for and treating sleep-disordered breathing (SDB) could reduce the risk of Alzheimer disease, especially for older individuals who are asymptomatic.

A team, led by Gaël Chételat, PhD, director of research, the French National Institute of Health and Medical Research, found data suggesting SDB increases the risk of Alzheimer disease due to its link with amyloid deposition and neuronal activity in Alzheimer-associated brain regions, most notably the posterior cingulate cortex and precuneus.

These links could explain why sleep-disordered breathing is tied to an increased risk for developing Alzheimer clinical syndrome at a younger age.

The assessment, dubbed the Age-Well clinical trial, included 137 participants, of which 127 were included for analysis. The mean age was 69.1 (standard deviation [SD], 3.9) years, and 63% (n = 80) were women.

Using the apnea-hypopnea index (AHI) value, the participants were divided into a group with SDB (AHI <15 events per hour, n = 31) and those without SDB (AHI ≥15 events per hour, n = 96).

To determine which aspect of SDB severity is most closely linked to these brain changes, the investigators performed forward stepwise regressions. The analysis reported that hypoxia composite score (unstandardized β, 0.06 [95% CI, 0.02—0.10]; P = .002), followed by APOE4 status (unstandardized β, 0.07 [95% CI, 0.001—0.14]; P = .05), which explained 8% and 4% of the variance, respectively, were most strongly associated with amyloid burden.

The AHI value was the only variable associated with gray matter volume, explaining 4% of the variance (unstandardized β, 0.01; P = .04).

Amyloid burden was notably greater in those with SDB than those without (t117 = 4.51; familywise error corrected P = .04; Cohen d = 0.83), as well as gray matter volume (t119 = 4.12; P = .001; Cohen d = 0.75).

In addition to those, perfusion (t116&thinsp;=&thinsp;4.62; familywise error—corrected P&thinsp;=&thinsp;.001; Cohen d, 0.86) and metabolism (t79&thinsp;=&thinsp;4.63; familywise error—corrected P&thinsp;=&thinsp;.001; Cohen d, 1.04) were greater and overlapped primarily over the posterior cingulate cortex and precuneus.

“Interestingly, there was an overlap between brain changes observed in all 4 neuroimaging modalities over the posterior cingulate cortex, the precuneus, and the cuneus,” the authors wrote.

The perfusion, metabolism, and gray mater volume signal values, extracted from significant clusters, showed strong intercorrelations (perfusion-metabolism: Pearson’s r = 0.70 [95% CI, 0.58—0.80]; P <.001; perfusion-gray matter: r = 0.59 [95% CI, 0.46—0.69]; P <.001; metabolism-gray matter: r = 0.40 [95% CI, 0.21—0.56]; P <.001). As well, amyloid deposition was significantly correlated with both gray matter volume (r = 0.21 [95% CI, 0.03—0.37]; P = .02) and perfusion (r = 0.34 [95% CI, 0.18—0.49]; P <.001).

There was no association observed with cognition, self-reported cognitive and sleep difficulties, or excessive daytime sleepiness symptoms.

“We believe that these overlapping patterns reinforce the likelihood of common underlying mechanisms. Indeed, it has been demonstrated that higher neuronal activity is associated with increased β-amyloid production,” the authors wrote. “In addition, several studies have shown that neuroinflammatory processes play a central role in Alzheimer disease progression and are associated with higher levels of amyloid deposition. Thus, SDB-associated neuroinflammatory processes and associated neuronal hyperactivity are likely to promote amyloid deposition in the same area.”

No variable was significantly associated with brain perfusion or metabolism, which means early neuroinflammatory and neuronal hyperactivity processes promoting amyloid deposition could represent the underlying mechanisms increasing the susceptibility to Alzheimer disease at an asymptomatic stage of sleep disordered breathing.

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