From Baptist Health South Florida
3 min. read
Research on the brains of patients with Alzheimer’s disease has uncovered toxic proteins that interrupt signals firing between neurons. Those signals play an important role in cognitive function and memory. When the signals are altered by a sticky plaque, made up of the toxic protein amyloid, the resulting cognitive deterioration is known as Alzheimer’s.
Now, new research published in the July 5 edition of the journal Neurology, indicates that sleep disturbances may lead to a buildup of amyloid in the brains, indicated by biomarkers present in the cerebrospinal fluid, of some people at risk for developing Alzheimer’s.
Study participants had a higher risk of Alzheimer’s disease due to either the presence of a gene mutation or a positive family history of the disease. Those who reported poor sleep quality had a higher level of the biomarker for amyloid in their spinal fluid, compared with those who did not report having trouble sleeping.
“We’ve known for some time that Alzheimer’s patients have sleep disorders, such as insomnia and changes in their circadian rhythm that result from deposits of amyloid in the brain’s sleep centers,” said neurologist and sleep specialist David Seiden, M.D., medical director of the Baptist Sleep Center at Pembroke Pines. “But this study suggests there may be some bi-directionality to the relationship between sleep quality and the development of Alzheimer’s in certain at-risk populations. That is, sleep disturbances may predispose certain patients to Alzheimer’s.”
The interest in the link between sleep and Alzheimer’s stems from a study published in 2013 that revealed a waste-removal system in the brains of mice that was activated during sleep. This “glymphatic system” pushed amyloid protein from the spaces between brain cells into the cerebrospinal fluid for elimination as waste.
A study published in 2015 tested the brains of patients between the ages of 56 and 68 using PET-scan imaging to determine the amount of amyloid in certain areas of the brain. Similar to this latest study of cerebrospinal fluid, the 2015 study found that those patients whose sleep was less adequate, based on subjective measurements, had greater amounts of amyloid accumulation in their brains. This finding led researchers to want to determine whether poor sleep may be a risk factor for Alzheimer’s. They also want to find out if such an early indicator of Alzheimer’s can lead to preventive treatment before there is cognitive deterioration.
“What these studies show us is that poor sleep may be a modifiable risk factor to prevent the development of Alzheimer’s,” Dr. Seiden explained. “We can’t make the leap to ‘sleeping better will prevent Alzheimer’s disease,’ but there’s mounting evidence to suggest the correlation between sleep and Alzheimer’s that requires further study.”
Dr. Seiden warns that this latest study relies on patients’ own subjective input regarding their sleep quality. A better approach, he says, would be to measure the quality of a person’s sleep in the Sleep Lab. The data would better determine whether people with poorer sleep quality, based on objective measurements, have increased levels of the amyloid biomarker in their cerebrospinal fluid. Moreover, the following question would need to be answered: Does improvement in sleep quality improve the efficiency of the glymphatic system to clear out amyloid from the brain, and therefore, decrease the risk of Alzheimer’s disease?
“This study speaks to the increasing evidence that improved quality and quantity of sleep leads to better health,” Dr. Seiden said. “Studies have shown that poor sleep quality puts people at higher risk for diabetes, depression, high blood pressure, obesity, cancer and premature death. Soon, we may be adding Alzheimer’s disease to that list. For now, this is additional data to support the importance of quality sleep.”
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