A recent study has discovered that individuals with severe sleep-disordered breathing, which includes conditions like heavy snoring and sleep apnea, exhibit shrinkage in a region of the brain connected to memory. Sleep apnea is characterized by repeated instances of interrupted breathing for 10 seconds or more during sleep.
The study’s lead author, Géraldine Rauchs, a postdoctoral research officer at the National Institute of Health and Medical Research in Caen, France, highlighted the connection between untreated sleep disorders and an increased risk of dementia. The researchers focused on the medial temporal lobe, an area of the brain that is particularly vulnerable to Alzheimer’s disease.
The medial temporal lobe houses the hippocampus, a complex structure crucial for learning, memory encoding and consolidation, and spatial navigation. The study found that brain volume loss occurred only when individuals with sleep apnea also exhibited signs of beta-amyloid plaques, a key indicator of Alzheimer’s disease.
Rauchs explained that individuals without amyloid plaques did not experience a decrease in brain volume, even if they had severe sleep apnea. It is worth noting that amyloid buildup in the brain can begin as early as the 30s and 40s, long before the onset of cognitive decline. During sleep, especially deep, slow-wave sleep, the brain clears away a significant portion of amyloid buildup.
Rudy Tanzi, a professor of neurology at Harvard Medical School, emphasized that sleep apnea’s association with reduced brain volume in older individuals, particularly those with amyloid plaque, is logical. Improper removal of amyloid can trigger the development of Alzheimer’s pathology, eventually leading to dementia.
The study, published in the journal Neurology, involved 128 participants aged 65 and older who were part of the Age Well clinical trial in Caen, France. None of the participants had cognitive, psychiatric, or chronic diseases at the study’s outset, and those who developed sleep-disordered breathing and received continuous positive airway pressure (CPAP) treatment were excluded.
The results showed that 91 out of 122 participants had moderate to severe sleep apnea. Only 11 participants reported excessive daytime sleepiness. Among the participants, 26 had amyloid plaques, and in those individuals, severe sleep-disordered breathing was linked to reduced volume in the medial temporal lobe. The degree of volume loss correlated with the severity of sleep apnea.
Additionally, the study found that lower volumes in specific regions of the medial temporal lobe were associated with worse memory performance assessed 18 months later. Notably, no brain volume shrinkage was observed in individuals with sleep apnea who did not have amyloid plaques, suggesting that certain individuals may be more susceptible to the negative effects of breathing-related sleep disorders.
According to estimates, approximately 936 million adults worldwide between the ages of 30 and 69 may suffer from sleep apnea, with many cases going undiagnosed. Severe and untreated sleep apnea increases the risk of mortality by threefold. Previous studies have shown a connection between sleep apnea and brain damage, white matter lesions, thinning brain matter, and impaired memory and recall.
Rauchs’s prior research indicated that amyloid burden in the brain is predicted by the severity of hypoxia associated with sleep apnea. Hypoxia refers to the lack of oxygen to the brain during episodes of breathing cessation. Regions of the medial temporal lobe, including the hippocampus, are particularly vulnerable to hypoxia.
These findings emphasize the importance of consulting a sleep specialist and receiving treatment for sleep apnea to maintain a healthy brain and reduce the risk of amyloid deposits and subsequent Alzheimer’s pathology, which can lead to cognitive decline.