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“Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways,” said Barbara B Bendlin from the University of Wisconsin-Madison in the US.
“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,” said Bendlin. Amyloid is a protein that can fold and form into plaques. Tau is a protein that forms into tangles. These plaques and tangles are found in the brains of people with Alzheimer’s disease.
Researchers recruited 101 people with an average age of 63 who had normal thinking and memory skills but who were considered at risk of developing Alzheimer’s, either having a parent with the disease or being a carrier of a gene that increases the risk of Alzheimer’s called apolipoprotein E or APOE. Participants were surveyed about sleep quality. They also provided spinal fluid samples that were tested for biological markers of Alzheimer’s disease.
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Those biological markers included signs of amyloid, tau and brain cell damage and inflammation.“It is important to identify modifiable risk factors for Alzheimer’s given that estimates suggest that delaying the onset of Alzheimer’s disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 5.7 million and save USD 367 billion in health care spending,” said Bendlin. While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid, researchers said. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea. The results remained the same when researchers adjusted for other factors such as use of medications for sleep problems, amount of education, depression symptoms or body mass index.
The study was published in the journal Neurology.