Sleep and Alzheimer’s – Are They Related?
New research published in the online July issue of Neurology, a prestigious medical journal from the American Academy of Neurology, noted that people with sleep disorders who are otherwise healthy might be more prone to develop Alzheimer’s disease than those who do not have any sleep problems. Researchers identified a connection between biological markers for Alzheimer’s and sleep disorders. This link was found in the spinal fluid.
Dr. Barbara B. Bendlin from the University of Wisconsin-Madison and lead author of the study noted that prior research had shown possible connections between sleep disturbances and the progression or development of Alzheimer’s disease. For instance, old studies found that sleep deprivation may lead to amyloid plaque buildup – a sign of Alzheimer’s disease on brain imaging – because amyloid plaque can only be cleared out by the brain during sleep. This recent study focused on both amyloids, as well as other biological markers in the cerebrospinal fluid.
The protein, amyloid, turns into plaque by folding itself over. Another protein identified in this research is tau, which forms and folds into knots. Both proteins in their relative plaque or tangle formation are found on brain imaging of Alzheimer patients.
In this recent study, scientists enlisted 101 individuals who were thought to be at risk of developing Alzheimer’s disease due to a family history of the condition or having a carrier gene called apolipoprotein E or APOE, which is thought to be an indicator for Alzheimer’s. Participants were an average age of 63 years and had normal memory and thinking skills. Participants filled out surveys about sleep quality and provided consent for spinal fluid samples, which the lab tested for the known biological markers of Alzheimer’s.
Scientists discovered that those who had more sleep problems, excessive daytime sleepiness, and poor sleep quality were more likely to have excess biological markers for Alzheimer’s disease in their spinal fluid sample than those who reported no sleep problems at all. The specific markers related to Alzheimer’s included tau, amyloid, and brain cell inflammation and damage.
Dr. Bendlin notes that it is critical to identify risk factors for Alzheimer’s disease since recent estimates indicate that delaying the onset of the disease even by just five years could significantly reduce the number of Alzheimer’s cases by almost 6 million over the next 30 years. This would save approximately $367 billion dollars in annual health care spending.
Of important note is that not everyone who reported sleep problems had spinal fluid abnormalities. The links were compelling when looking at the correlation as a group, but not so much on an individual basis. For instance, there was no connection between obstructive sleep apnea and high biological markers in the fluid sample.
Even after adjusting for factors like the use of sleep medications, education levels, mental health, and body mass index, results were the same.
While researchers are still uncertain if sleep is affecting Alzheimer’s disease development or progression, or if the illness itself is responsible for the sleep problems, they are still hopeful that additional research will lead to further discovery of the link between Alzheimer’s markers and sleep.
Dr. Bendlin noted in her report that there are currently many ways to improve sleep, so this should be a good early intervention tactic for people who are at risk of developing Alzheimer’s disease. Improving sleep may help delay the onset of the condition.
One of the limits of this research was that the participants reported all sleep problems and not by a medical professional or a review of medical records. A critical component of future studies will have a health professional monitor sleep patterns in addition to the self-reporting.
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