If you don’t do this while you sleep, it can be disastrous for your brain

Although dementia is most commonly associated with memory impairment, the term actually refers to a wide array of neurodegenerative effects. Among these is excessive or insufficient sleep.

And just like dementia’s correlating diseases impact a healthy sleep regimen, a healthy sleep regimen has been studied to delay cognitive decline as we age.

The research literature suggests that beta-amyloid, which is the metabolic waste that accumulates between neurons, gets cleared out during phases of deep sleep.

Ladders recently reported on the increased levels of tau tangles inside the brain cells of people with Alzheimer’s and other cognitive illnesses.

Similarly, if a buildup of beta-amyloid clumps into amyloid plaques, neurons become unable to successfully communicate with one another–leading to complications linked to dementia.

In a new study conducted on mice and human models, published in the journal Current Biology, researchers defined the relevant parameters more squarely, writing:

“Experimental sleep-wake disruption in rodents and humans causally modulates β-amyloid (Aβ) dynamics. This leads to the hypothesis that, beyond cross-sectional associations, impaired sleep structure and physiology could represent prospective biomarkers of the speed with which Aβ accumulates over time. Here, we test the hypothesis that initial baseline measures of non-rapid eye movement (NREM) sleep slow-wave activity (SWA) and sleep quality (efficiency) provide future forecasting sensitivity to the rate of Aβ accumulation over subsequent years.”

Miraculously, by the end of the analysis, the authors were able to produce a model that can potentially predict the amount of beta-amyloid buildup one is going to accumulate over the next few years based on their current sleep schedule.

“There is something about this deep sleep that is helping protect you,” explained Matthew Walker, a professor of neuroscience and psychology at the University of California, Berkeley who worked on the new report in a release. “The research comes after decades of observations linking poor sleep to long-term problems with memory and thinking. We are now learning that there is a significant relationship between sleep and dementia, particularly Alzheimer’s disease.”

Walker and his team accompanied preliminary results with a sample comprised of otherwise healthy older adults.

Each was examined via objective sleep polysomnography alongside longitudinal tracking of Aβ accumulation with PiB positron emission tomography (PET) imaging.

The results were pretty clear. Deep sleep serves as a disposal period for waste products associated with Alzheimer’s disease–more directly, beta-amyloid and tau.

“Both the proportion of NREM SWA below 1 Hz and the measure of sleep efficiency predicted the speed (slope) of subsequent Aβ deposition over time, and these associations remained robust when taking into account additional cofactors of interest (e.g., age, sex, sleep apnea),” the authors conintued. “Moreover, these measures were specific, such that no other macro- and microphysiological architecture metrics of sleep demonstrated such sensitivity.”

Deep sleep denotes the slowest brain wave sleep stage. In addition to the purported benefits indexed above, this sleep stage is said to provide energy restoration, cell regeneration, increases blood supply to muscles, facilitate the growth of tissues and bones and strengthen our immune system.

Not too long back, Ladders interview a trauma specialist who determined deep sleep to help sexual assault survivors heal emotional wounds.

It thus stands to reasons, that the same phase induces the removal of toxic products like amyloid beta and tua, that contribute to cognitive unwellness.

“Our data support the proposal that objective sleep markers could be part of a set of biomarkers that statistically forecast the longitudinal trajectory of cortical Aβ deposition in the human brain,” the author concluded. “Sleep may therefore represent a potentially affordable, scalable, repeatable, and non-invasive tool for quantifying of Aβ pathological progression, prior to cognitive symptoms of Alzheimer’s disease.”