Cognitively healthy adults whose sleep quality declined in middle age were more likely in late life to accumulate Alzheimer’s disease-related proteins in the brain than those whose sleep quality improved or did not change, an NIA-supported study found. Researchers at the University of California, Berkeley, suggest that sleep assessment could one day be used as a noninvasive, inexpensive predictor of Alzheimer’s risk.
It’s also possible that treating sleep problems during “windows of sensitivity” in middle age might help delay the progression of the disease, according to the study, published in the Journal of Neuroscience.
The researchers analyzed 101 older adults, enrolled in the Berkeley Aging Cohort Study, for beta-amyloid and tau levels, as shown by positron emission tomography (PET) scans. Accumulation of beta-amyloid and tau proteins are common predictors of Alzheimer’s dementia. The researchers also assessed sleep quality: 31 participants completed an electroencephalogram (EEG) sleep assessment, and 95 completed a questionnaire about previous changes in sleep duration and quality.
In participants who had undergone an EEG, fewer slow brain waves during deep sleep were significantly associated with increased beta-amyloid levels in the cortex, the brain’s information processor. Another sleep activity—the interaction of slow brain waves and brief bursts of activity, called spindle oscillations—was strongly associated with increased tau in the medial temporal lobe, a brain region important for long-term memory, the researchers found.
In addition, shorter sleep duration was associated with Alzheimer’s-related brain changes later in life, the researchers found. Specifically, participants who reported shorter sleep in their 50s or their 70s had significantly more beta-amyloid in later life than those whose sleep did not decline. Similarly, participants who reported shorter sleep in their 60s had significantly more tau in later life compared with those whose sleep increased or stayed the same.
These findings help establish that changes in sleep quality and quantity in middle age are associated with, and sometimes predict, Alzheimer’s-related brain changes. However, it is unclear if sleep impairment causes these brain changes, or vice versa. Further studies in larger groups of people could clarify the timing of changes in sleep quality and accumulation of beta-amyloid and tau in the brain.
This study was supported by NIA grants R01AG031164, RF1AG054019, RF1AG054106, and F32AG057107.
Reference: Winer JR, et al. Sleep as a potential biomarker of tau and β-amyloid burden in the human brain. Journal of Neuroscience. 2019;39(32):6315-6324. doi: 10.1523/JNEUROSCI.0503-19.2019.