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Sleep disruption is linked with the pathophysiology of Alzheimer’s disease, with characteristic changes in sleep emerging early in life, well before the clinical onset of the disease. A key player in the development of Alzheimer’s disease is amyloid-beta. Insufficient sleep increases the production of amyloid-beta, and amyloid-beta deposition, in turn, impairs sleep in a vicious, self-perpetuating loop. Findings from a new study demonstrate that chronic poor sleep predicts the degree of amyloid-beta deposition in the brain.

The study involved 32 older adults (average age, 73 years) who were cognitively intact. The authors of the study analyzed the participants' sleep patterns at the beginning of the four-year study. At periodic intervals throughout the study, the authors measured the participants' cognitive function and performed positron emission tomography (PET) scans to check for the presence of amyloid-beta in the participants' brains.

They found that most of the participants already had some amyloid-beta accumulation in their brains, but this was not surprising, considering the participants' ages. They also found that participants who had less slow wave sleep and poor sleep efficiency were more likely to have faster accumulation of amyloid-beta.

These findings demonstrate that objective markers of sleep could forecast the rate of amyloid-beta deposition in the human brain.

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