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First time the correlation has been measured in adults with normal cognition
Madison, Wis. — Older adults who slept poorly and often felt tired also had higher deposits of amyloid plaques in the brain, a condition thought to mark the beginning of Alzheimer’s disease.
A study led by a multi-disciplinary team of University of Wisconsin-Madison researchers from the Alzheimer’s Disease Research Center and the Center for Sleep Medicine and Sleep Research suggests that poor sleep in late middle age could be one of the first symptoms of Alzheimer’s disease. But senior author Dr. Ruth Benca notes that, despite the correlation, the study doesn’t show whether poor sleep causes the amyloid plaques to develop in the brain, or whether amyloid plaques prevent quality sleep.
Lead author Kate Sprecher, a doctoral student in the UW Neuroscience Training Program, studied positron emission tomography (PET) scans to look for amyloid plaque in the brains of 98 adults, ages 50 to 73, who had normal cognitive skills and no symptoms of dementia. The participants are part of the long-running Wisconsin Registry for Alzheimer’s Prevention (WRAP) study, which is tracking 1,500 people to determine risks for developing the disease.
She found that a higher burden of amyloid plaque was strongly associated with people reporting greater sleepiness or difficulty sleeping. While it will take more research to determine whether amyloid build-up leads to poor sleep or vice versa, Sprecher says it’s the first time the connection has been noted in younger people who don’t yet show signs of cognitive decline.
“If it turns out that poor sleep is causing amyloid to build up, then improving the quality of sleep could be a way of slowing the disease progression,” Sprecher says. “We already have a number of effective clinical strategies for treating sleep disorders and improving sleep.”
Conversely, sleepiness could be an “early warning” that amyloid is beginning to build up, opening an earlier window for treatment that could be more successful. Current treatments generally begin after cognitive decline and are not very effective. Benca emphasized that poor sleep should not necessarily be considered a part of “normal” aging and that addressing sleep issues should be part of regular health care evaluations, particularly in older adults.
Benca and Sprecher both praised the data available via the Wisconsin Alzheimer Institute’s WRAP data base and plan further studies with the ADRC to see if the sleep disturbances correlate with the progression of the disease.
“The sleeping brain gives us a unique window on aging,” says Benca.
Coauthors on the study include Drs. Barbara B. Bendlin; Ozioma C. Okonkwo, Bradley T. Christian; Rebecca L. Koscik, Mark A. Sager and Sterling C. Johnson, who are associated with the Geriatric Research Education and Clinical Center at the William S. Middleton Memorial VA Hospital, the Wisconsin Alzheimer’s Disease Research Center and the Wisconsin Alzheimer’s Institute.
The study was published in the journal Neurobiology of Aging and is available here: http://www.neurobiologyofaging.org/article/S0197-4580%2815%2900251-1/abstract