An international team of researchers led by scientists at the University of Wisconsin-Madison found that people who experienced poor sleep in late midlife also had brain characteristics that point to an increased risk for developing Alzheimer’s disease.
The study, “Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults,” was published online in Neurology, the medical journal of the American Academy of Neurology. Dr. Barbara Bendlin, an associate professor of medicine (geriatrics) and an Alzheimer’s disease researcher at the UW School of Medicine and Public Health and Dr. Kate Sprecher, neuroscience researcher at UW, led the study.
The study supports a growing body of evidence that links sleep quality and Alzheimer’s disease.
“Our findings suggest that improving sleep during mid-life could potentially reduce a person’s risk of Alzheimer’s disease. While it’s not the case that everyone with sleep problems will develop Alzheimer’s disease, sleep disturbance is a common, treatable issue for many middle-aged Americans. Sleep medicine may represent a promising, untapped toolkit for preventing or delaying Alzheimer’s disease,” Sprecher said.
The research looked at the link between self-reported sleep patterns and early indicators of Alzheimer’s disease in the brain, including amyloid plaque and tau protein levels, as well as markers of inflammation and brain-cell injury.
The study included 101 volunteers between the ages of 57 and 69; all had normal memory. Participants were recruited from the Wisconsin Registry for Alzheimer’s Prevention, a group of more than 1,500 volunteers, most of whom have a parental risk for Alzheimer’s disease and who take part in research studies on Alzheimer’s disease. Study volunteers answered a questionnaire about their sleep habits.
Researchers also examined the levels of proteins related to Alzheimer’s disease in research volunteers’ cerebrospinal fluid (CSF). This fluid surrounds the brain and spinal cord and carries a multitude of indicators of a person’s brain health.
“Participants in our study who reported more sleep problems, including inadequate sleep, greater daytime sleepiness and more sleep problems, showed signs of more amyloid being deposited in the brain. Amyloid deposits in the brain are a hallmark of Alzheimer’s disease,” said Bendlin. “Dr. Sprecher also examined markers related to brain-cell injury and activity of cells that respond to injury, and these were also associated with subjective reports of sleep quality.”
More than five million Americans have Alzheimer’s dementia, a number that is expected to triple by 2050 without medical advancements to slow, stop, or treat the disease. The Alzheimer’s Association predicts that delaying the onset of dementia symptoms in people at risk for the disease by five years would reduce Alzheimer’s disease cases by 5.7 million and save $367 billion in health care spending in the United States.
Co-authors of the study from the University of Wisconsin include Dr. Rebecca Koscik and Dr. Mark Sager from the Wisconsin Alzheimer's Institute; Dr. Cynthia Carlsson, Dr. Ozioma Okonkwo, Dr. Sanjay Asthana and Dr. Sterling Johnson, all affiliated with the Wisconsin Alzheimer's Disease Research Center and Wisconsin Alzheimer’s Institute at the University of Wisconsin-Madison, and the Geriatric Research Education and Clinical Center at William S. Middleton Memorial Veterans Hospital. The research team also included investigators from the University of Gothenburg in Mölndal, Sweden and the University of California, Irvine.
This research was funded by grants R01 AG027161, R01 AG021155, ADRC P50 AG033514, R01 AG037639 and National Research Service Award F31 AG048732 from the National Institute on Aging, and by the Clinical and Translational Science Award (CTSA) program, through the NIH National Center for Advancing Translational Sciences (NCATS), grant UL1TR000427.