Commentary on NPR article, contributed by Bryce Mander, PhD
Numerous studies now show that multiple forms of sleep disturbance increase risk for developing dementia.
Emerging work continues to demonstrate that the way in which the brain expresses sleep may be tied to how much Alzheimer’s disease (AD) pathology there is in the brain even prior to AD symptom onset.
Both sleep restriction and suppression of high amplitude, low frequency brain waves – called slow waves – during deep sleep increase beta amyloid and tau, the two hallmark pathologies of AD. It is unknown how this occurs, though there is evidence of two potential mechanisms:
- increased production of AD pathologies in the brain, or
- decreased clearance of AD pathologies from the brain through its slow wave-regulated glymphatic system.
Further compounding this effect, increased burden of these pathologies can also disrupt sleep expression even before beta amyloid plaques are formed in the cortex, an initial feature of AD pathogenesis.
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As described on NPR, a study my colleagues at UC Berkeley and I published this month in Current Biology indicates that a specific deficit in the expression of the lowest frequency slow waves can predict how much beta amyloid pathology will be present in the brain 2-6 years later in older adults with no cognitive symptoms. Though less powerfully, how much sleep was fragmented also predicted future beta amyloid burden.
These findings are important, because they demonstrate that specific measures of sleep expression may be able to predict which individuals are on the way to developing AD pathology before clinically significant symptoms are observed. This could ultimately aid intervention efforts targeting AD prevention. I review this literature and these findings in depth in a recent review published in Frontiers in Neuroscience.
A critical next step will be to determine whether manipulating these sleep features to improve sleep quality will impact the accumulation of AD pathologies and reduce AD risk. This is an important research question for multiple researchers at UCI MIND, and is a core research mission for the UCI Sleep and Circadian Neuroscience (SCN) center sponsored by the UCI Office of Research.
Individuals interested in participating in our upcoming studies of sleep and AD can enroll in the UCI Consent-to-Contact (C2C) Registry. It is only through our partnership with volunteers in the community that we can continue to pave the way for new treatments and cures for those suffering from debilitating diseases such as AD.
Bryce Mander, PhD, is Assistant Professor of Psychiatry & Human Behavior at UCI. He received his PhD in Neuroscience at Northwestern University, and completed his postdoctoral fellowship in the Department of Psychology at UC Berkeley. His research looks at how sleep disturbance impacts brain function, thinking, and memory in older adults, particularly those at risk for dementia. In his studies, he combines the use of multiple brain imaging tools, such as MRI, EEG, and PET, with behavioral testing to uncover the mechanisms linking sleep disturbance to cognitive decline in later life. Dr. Mander is one of the fields leading experts in the neuroscience of sleep and has published many important findings on the link between sleep and brain health.
