Researchers found that the more severe people’s obstructive sleep apnea, the more likely they are to have a higher burden of beta-amyloid plaques in the hippocampus.
The Greek word “apnea” means “without breath.” Sleep apnea is a medical condition that impacts breathing during sleep, and the most common type, obstructive sleep apnea, affects up to roughly one in three older adults. People with the condition stop breathing for brief periods during sleep due to the narrowing or closing of the airway as their muscles relax. Beyond the problems of loud snoring and poor quality of sleep, obstructive sleep apnea may also tell us something about the brain.
According to Dr. Stephen Robinson, a researcher and professor at RMIT University in Australia who studies the connection between sleep apnea and cognitive function, scientists know there is a strong link between cognitive function and sleep apnea, that people who have sleep apnea in mid-life are more likely to develop Alzheimer’s when they are older. In addition, those who have Alzheimer’s are more likely to have sleep apnea than other people their age. “The connection is there,” he said in a news release, “but untangling the causes and biological mechanisms remains a huge challenge.”
In a recent study published in the journal Sleep, Robinson and colleagues made progress in unraveling that mystery.
“Our study is the first to find Alzheimer’s-like amyloid plaques in the brains of people with clinically-verified obstructive sleep apnea,” Robinson said. “It’s an important advance in our understanding of the links between these conditions and opens up new directions for researchers striving to develop therapies for treating, and hopefully preventing, Alzheimer’s disease.”
Past research has shown that obstructive sleep apnea may damage the brain, and people can develop significant cognitive impairment. Scientists also understand that just like people with Alzheimer’s, people with severe obstructive sleep apnea can suffer from atrophy of the hippocampus, a brain region central to memory. While it was unclear whether such atrophy is accompanied by one of the hallmarks of Alzheimer’s — beta-amyloid plaques — scientists in the recent study are closing this gap of knowledge.
The team analyzed the post-mortem hippocampi of 34 people with obstructive sleep apnea, and the area of the brain which regulates sleep, heart rate and breathing, known as the brainstem, of 24 people with the condition.
The researchers found that the more severe people’s obstructive sleep apnea, the more likely they were to have higher burdens of beta-amyloid plaques in the hippocampus. While none of the participants were diagnosed with Alzheimer’s, the researchers suggested that some of them may have had undiagnosed Alzheimer’s or mild cognitive impairment, a clinical syndrome which can be associated with the early stages of Alzheimer’s.
The researchers wrote that obstructive sleep apnea is neither “sufficient nor necessary” to cause Alzheimer’s. Instead, they suggested that obstructive sleep apnea may accelerate the disease. Episodes of oxygen deprivation followed by re-oxygenation, may lead to stress that injures the hippocampus and brain regions nearby, rendering them more vulnerable to the ravages of Alzheimer’s disease.
They also posited that deficiency in deep sleep of people with obstructive sleep apnea may hinder their brain’s ability to clear beta-amyloid from the brain. And past research has shown that the brain’s glymphatic system comes into play during sleep, clearing waste and cycling glucose, lipids and amino acids.
Robinson and the team will continue to analyze the brain sample to better understand other factors that may be involved, including inflammation and changes to the blood vessels that supply nutrients to the brain.
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