At least as early as 2017, scientists have recognized that during deep sleep—also known as slow-wave sleep (SWS) because of its characteristic slow brain wave activity—the brain sweeps out amyloid proteins that accumulate as waste products from brain cell (neuron) activity. But it wasn’t until this year that scientists have been able to actually see the cleaning process in action using MRI and electroencephalograms. During the study, published in this November’s edition of Science, researchers were able to actually see the cerebrospinal fluid (CSF) washing into the brain and flushing out toxic amyloid waste every 20 seconds or so.
According to Laura Lewis, an assistant professor in the department of biomedical engineering at Boston University and the study’s lead author, “Before each wave of fluid, we would actually see a wave of electrical activity in the neurons. This electrical wave always happens first, and the CSF wave always seems to follow seconds later.” Her team concluded that the slow neuron activity and the resulting decrease in blood flow trigger the cleansing pulses of CSF.
Highly Choreographed Cleansing during Deep Sleep
The slow waves of electrical activity that define deep sleep mark a decrease in brain activity. Neurons go quiet after the slow electrical wave, and because they are not firing, they need less oxygen, so less blood flows through the brain. Less blood means more space for the waste removal process.
Lewis’s team was able to observe that CSF rushed in to fill the void left by the ebbing blood flow immediately following each pulse of the slow electrical wave. As the flow of blood decreased, the flow of CSF increased, indicating the slow wave activity triggers a sequence of events designed to maximize the amount of amyloid toxins of than can be removed with each flush of CSF.
Research Builds on Prior Discoveries
Scientists believe that Alzheimer’s is caused by a build-up of beta-amyloid and tau proteins that clump together to form tangles and plaques that cause the widespread cell death that leads to Alzheimer’s. A study published in Science in 2013, showed that amyloid plaques were cleared away during sleep in mice. Furthermore, some studies also demonstrate that amyloid proteins build-up and form plaques when deep sleep is interrupted. But until Lewis’s study, no one knew why. The work of Lewis’s team demonstrates that sufficient deep sleep is necessary to clear the brain of the amyloid proteins that form the brain deteriorating plaques of Alzheimer’s.
New Research Opens New Avenues for Treatment
In 2013 Carla Shatz, professor of neurobiology and biology at the Stanford University School of Medicine, led a study suggesting that research into preventing Alzheimer’s needs to steer in a new direction. Her study, published in the journal Science in 2013, demonstrated that beta-amyloid begins destroying synapses (contact points where neurons relay signals to each other) long before the amyloid build-up forms plaques and people begin showing signs of the memory loss associated with Alzheimer’s.
Her team’s findings offer an explanation for the failures of recent large-scale clinical trials of therapies designed to slow the progression of Alzheimer’s. These treatments focus on ridding the brain of amyloid plaques after they have formed. Shatz’s research shows that the damage that leads to memory loss and other deteriorating functions has already been done by the time plaques develop, signaling a need for treatments that intervene in the earlier stages of the disease.
Dr. Lewis’s findings offer a new strategy for pre-emptive Alzheimer’s therapies. Restoring adequate SWS functions—and thus increasing the amount of CSF washing over the brain—may be the key to actually preventing the formation of amyloid plaques long before memory loss is apparent and the neurodegeneration associated with Alzheimer’s has begun.
While further research is clearly necessary to conclude that adequate sleep will prevent Alzheimer’s, Lewis’s study certainly suggests yet another reason to prioritize high quality sleep.