Insufficient sleep is a major public health issue, as the Centers for Disease Control and Prevention (CDC) caution. The CDC also estimate that between 50 and 70 million people in the United States have a “sleep or wakefulness disorder,” and they warn of the wide range of health problems that such disorders can trigger.
In addition to more intuitive negative health outcomes, such as poor quality of life and low productivity, sleeplessness puts people at risk of diabetes, depression, high blood pressure, and obesity, as well as cancer and premature death.
Recent research has added another condition to the list: Alzheimer’s disease. A study published last year shows how sleeplessness can interfere with the brain’s “glymphatic system,” which is a cleaning procedure that takes place during sleep, when cerebrospinal fluid flushes away unnecessary proteins and waste from the spaces between neurons.
Now, new research published in Neurology reveals a link between sleep disturbances and biological markers for Alzheimer’s disease.
Co-author Barbara B. Bendlin, Ph.D., of the University of Wisconsin-Madison, explains the motivation for the study, saying, “Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways.”
“For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain’s clearance system kicks into action during sleep. Our study looked not only for amyloid but for other biological markers in the spinal fluid as well.”
The researchers examined 101 people, all of whom were deemed at risk of developing Alzheimer’s disease either because they had a parent with the illness or because they had the apolipoprotein E gene, which put them at a higher risk.
The participants were 63 years old on average and had normal cognitive skills. They were asked to respond to a survey regarding the quality of their sleep, as well as to provide spinal fluid samples.
Biological markers for Alzheimer’s disease include signs of amyloid and tau protein buildup. Amyloid and tau are “sticky” proteins produced in excess in the brains of people with Alzheimer’s disease.
The former builds up into plaques, while the latter forms tangles. These are formations that either block the communication between neurons, or obstruct the transport of nutrients to nerve cells, eventually leading to neurodegeneration.
Upon analysis, participants’ cerebrospinal fluid showed “signs of amyloid, tau, and brain cell damage and inflammation.”
The results remained even when the researchers adjusted for potential confounders, including the use of sleep medication, education, depression, and body mass index (BMI).
However, the authors note that not all sleep disorders correlated with signs of Alzheimer’s. For instance, the researchers found no association between spinal fluid biological markers and obstructive sleep apnea.
“It’s important to identify modifiable risk factors for Alzheimer’s given that […] delaying [its] onset in people by a mere 5 years could reduce the number of cases we see in the next 30 years by 5.7 million.”
Barbara B. Bendlin, Ph.D.
The study did not address causality, so “it’s still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep. More research is needed to further define the relationship between sleep and these biomarkers.”
Dr. Bendlin concludes, “It may be possible that early intervention for people at risk of Alzheimer’s disease may prevent or delay the onset of the disease.”