Sleep apnea and Alzheimer’s linked to identical brain damage
Experts at RMIT University have discovered that sleep apnea patients have the exact same signs of brain damage as Alzheimer’s patients. The study has revealed that the severity of sleep apnea is reflected in the accumulation of amyloid plaques, which are known indicators of Alzheimer’s disease that are toxic to brain cells.
The researchers found that amyloid plaques develop in the same place and spread in the same way in the brains of people with obstructive sleep apnea and Alzheimer’s.
Study lead author Professor Stephen Robinson said scientists have known the two diseases are related, but what drives the connection is still unclear.
“We know that if you have sleep apnea in mid-life, you’re more likely to develop Alzheimer’s when you’re older, and if you have Alzheimer’s you are more likely to have sleep apnea than other people your age,” said Professor Robinson. “The connection is there but untangling the causes and biological mechanisms remains a huge challenge.”
“Our study is the first to find Alzheimer’s-like amyloid plaques in the brains of people with clinically-verified obstructive sleep apnea. 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.”
The team found that the build-up of amyloid plaques corresponded with the severity of sleep apnea. The research suggests that thc use of a continuous positive airway pressure (CPAP) machine made no difference in the amount of plaques found in the brain.
Individuals with obstructive sleep apnea (OSA) frequently stop breathing in their sleep due to a blockage of the airway. This disorder is becoming increasingly common and affects more than 936 million people worldwide.
Alzheimer’s is the most common form of dementia, and the biggest risk factor for developing the disease.
The researchers analyzed autopsy tissue from the hippocampus of 34 Alzheimer’s patients and from the brainstems of 24 people with OSA. While the experts found plaques in the brains of people with sleep apnea, the plaques were more strongly linked with severe sleep apnea.
“In cases of mild sleep apnea, we could only find plaques and tangles in the cortical area near the hippocampus, precisely where they are first found in Alzheimer’s disease,” said Professor Robinson.
The subjects had not displayed clinical symptoms of dementia before they died, suggesting they may have been in an early pre-dementia stage.
“While some people may have had mild cognitive impairment or undiagnosed dementia, none had symptoms that were strong enough for an official diagnosis, even though some had a density of plaques and tangles that were sufficiently high to qualify as Alzheimer’s disease,” said Professor Robinson.
“The next stage for our research will be to continue analyzing these samples to get a full understanding of the neuropathology, including signs of inflammation and changes to the blood vessels that supply nutrients to the brain.”
“The sample size for this study was limited, so we would also like to work towards establishing a clinical study with a larger cohort.”
The study is published in the journal Sleep.