Deposits of β-Amyloid (Αβ) plaques are one of the hallmarks of AD. Fluctuations in Αβ levels may be regulated by sleep-wake patterns, the authors write in the study background.
Adam P. Spira, Ph.D., of The Johns Hopkins Bloomberg School of Public Health, Baltimore, and colleagues used data from 70 adults (average age 76 years) in the Baltimore Longitudinal Study of Aging to examine whether self-reported sleep factors were associated with Αβ deposition, which was measured by imaging of the brain.
Study participants reported sleep that ranged from more than seven hours to no more than 5 hours. Reports of shorter sleep duration and lower sleep quality were both associated with greater Αβ buildup.
The authors acknowledge their study design does not allow them to determine whether sleep disturbance precedes Αβ deposition, so they are unable to say that poor sleep causes AD.
"In summary, our findings in a sample of community-dwelling older adults indicate that reports of shorter sleep duration and poorer sleep quality are associated with a greater Αβ burden. As evidence of this association accumulates, intervention trials will be needed to determine whether optimizing sleep can prevent or slow AD progression," the study concludes.