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A new study found that people with sleep apnea who are amyloid-positive are more likely to experience loss in brain volume and poorer scores on memory tests. FG Trade/Getty Images
  • Researchers investigated the link between sleep apnea, brain volume, amyloid-beta deposits, and memory.
  • They found that among people with sleep apnea, amyloid-positive individuals are more vulnerable to loss in brain volume and poorer scores on memory tests than their amyloid-negative counterparts.
  • Further studies are needed to understand what these findings mean for dementia pathology and potential treatments.

Sleep apnea is a sleep disorder that involves repeated stopping and starting of breathing during sleep, which can lead to low oxygen levels.

Studies show that sleep apnea may increase the risk of cognitive decline and dementia.

Research also shows that sleep apnea may exacerbate the buildup of amyloid beta proteins in the brain — a hallmark of Alzheimer’s disease (AD). Studies, however, have produced mixed results on how sleep apnea affects brain volume in the medial temporal lobe (MTL), which plays a key role in episodic memory and is typically atrophied in Alzheimer’s.

Gaining more insight into how sleep apnea affects brain volume is crucial for understanding more about the condition and its possible treatment avenues.

Recently, researchers investigated the link between sleep apnea severity, amyloid beta status, and brain volume in cognitively asymptomatic older adults.

They found that sleep apnea is linked to medial temporal lobe atrophy in adults with beta-amyloid buildup and that sleep apnea may increase their risk of memory impairment over time.

The study was published in Neurology.

For the study, the researchers recruited 122 cognitively asymptotic individuals with an average age of 69 years old.

To begin, they underwent a memory test, an at-home overnight sleep examination, and brain imaging, including an MRI scan and an amyloid PET scan. Memory tests were repeated an average of 21 months later.

The researchers noted that among the participants, 33 carried the ApoE4 gene — a genetic risk factor for AD — and 26 were amyloid-positive at baseline.

Amyloid-positive participants were more likely to be older and ApoE4 carriers, although they did not differ from amyloid-negative participants in terms of sex, education level, memory performance, medial temporal lobe volumes, and sleep data.

Ultimately, the researchers found that sleep apnea was linked to lower medial temporal lobe volumes in participants who were amyloid-positive, but not in those who were amyloid-negative.

The researchers wrote this suggests that some individuals may be more vulnerable to the adverse effects of sleep apnea than others.

They further found that lower hippocampal volumes at the beginning of the study were linked to worse episodic memory performance at follow-up.

In particular, they noted that females with significant levels of amyloid buildup were particularly vulnerable to adverse effects from sleep apnea, while males were less affected.

The findings remained after controlling for age, education, and ApoE4 status.

Medical News Today spoke with Dr. Howard Pratt, a board certified psychiatrist and medical director at Community Health of South Florida, not involved in the study, about why some people may be more vulnerable to the adverse effects of sleep apnea than others.

Dr. Pratt noted that whether sleep apnea and dementia are causally linked is uncertain at this point. He added that sleep apnea is nevertheless linked to diabetes, stroke, heart attack, and hypertension.

“When I speak with my patients, I always ask about their sleep,” Dr. Pratt said.

“Disordered sleep is a symptom of many conditions, so looking at overall health is key. Sleep apnea is a decrease in oxygen and an increase of carbon dioxide in [the] blood, which nightly over the years will have negative health consequences,” he added.

MNT spoke with Dr. Brendan Kelley, a neurologist and dementia expert with UT Southwestern’s O’Donnell Brain Institute, not involved in the study, about the limitations of the research.

Dr. Kelley noted that the findings are limited due to their small sample size and that as brain volume was not measured over time, it remains unknown whether untreated sleep apnea increases the risk of brain atrophy.

“Most of the group studied — 91 out of 122 people — had moderate or severe sleep apnea, and so it is difficult to determine whether people with brain amyloid who do not have sleep apnea show similar changes in brain volume. To get around this, the authors studied the severity of sleep apnea based on certain measurements during sleep. However, the lack of a group having no apnea is a limitation.”

– Dr. Brendan Kelley, neurologist and dementia expert

MNT also spoke with Dr. Paul E. Schulz, professor of neurology and director of the Neurocognitive Disorders Center with McGovern Medical School at UTHealth Houston, not involved in the study.

Dr. Schulz said that the study suggests sleep apnea may cause a change in either the accumulation of amyloid or affect hippocampal volumes via a different mechanism.

“We all make amyloid at the same rate. Those who get rid of it more slowly seem to be the ones that get AD. Sleep seems to be a time when amyloid is removed from the brain. Sleeping less seems to be associated with a greater risk for [Alzheimer’s]” he explained.

He noted that while the study doesn’t test this theory directly, it raises the possibility that sleep apnea may be a risk factor for Alzheimer’s by cleaning less amyloid, resulting in greater accumulation and then greater loss of hippocampal volume.

“That is my reading of the data, but this study doesn’t test that directly, of course. It just shows that [sleep apnea] is associated with smaller hippocampi.The mechanisms underlying the increased risk for hippocampal volume changes in the group with [sleep apnea] needs to be investigated further.”

– Dr. Paul E. Schulz, professor of neurology

While human studies are still needed to investigate this link, some research has produced findings that match Dr. Schulz’s theory. A recent mouse study found that sleep deprivation prevents immune cells known as microglia from cleaning up deposits of amyloid protein during the sleep cycle.

What exactly this means for Alzheimer’s progression requires further investigation.

In another recent study, researchers examined the effect of deep sleep in individuals who had not been diagnosed with dementia but who had higher levels of beta-amyloid in their brains.

The study authors found that deep sleep offset negative associations between high levels of beta-amyloid in the brain and memory. These findings, they wrote, suggest that good quality sleep may offset the negative effects of beta-amyloid accumulation by enhancing cognitive reserve- mental resilience during the aging process.

Dr. Aaron Ritter, psychiatrist and director of the Memory & Cognitive Disorders program at Hoag Hospital in Newport Beach, California, not involved in the study, told MNT:

“This research suggests that treating sleep apnea appears to be one of the most effective things a provider can do when treating individuals with Alzheimer’s disease.”

A common treatment for sleep apnea is Continuous positive airway pressure (CPAP) therapy, which involves wearing a mask while sleeping that provides a constant stream of positive air pressure.

Other interventions include lifestyle changes, including improved diet quality and sleeping on the side, medication, and surgery aimed at widening the airways.

“If you’re a person that is not sleeping well, or have been accused of snoring, tell your doctor. One of the most common symptoms of sleep apnea is waking up with a headache. When people get treated, they do very well. Some of my patients never realized they had rarely had a good night’s sleep until they received treatment.”

– Dr. Howard Pratt, psychiatrist