Could Brain Activity During Sleep Be a Biomarker for Alzheimer’s?
Could Brain Activity During Sleep Be a Biomarker for Alzheimer’s?

Could Brain Activity During Sleep Be a Biomarker for Alzheimer’s?

Changes in brain waves while snoozing correlate with accumulation of tau and amyloid-β, suggesting that the neural activity disruptions could clue doctors in to early development of the disease.

Oct 1, 2019
Ashley Yeager

ABOVE: © istock.com, WIKIMEDIA, PATHO

EDITOR’S CHOICE IN MICROBIOLOGY

The paper
J.R. Winer et al., “Sleep as a potential biomarker of tau and β-amyloid burden in the human brain,” J Neurosci, 39:6315–24, 2019.

Everybody sleeps, but not all sleep is created equal. Good sleep appears to keep the brain healthy, clearing toxins from the organ. But bad sleep might be a sign of neurodegenerative disease, with past studies linking sleep disturbances to the progression of Alzheimer’s disease. 

Interested in whether brain waves correlated to accumulation of tau and amyloid-β, two proteins considered hallmarks of the disease, University of California, Berkeley, graduate student Joseph Winer and colleagues took positron emission tomography measures of the proteins in 31 cognitively healthy individuals in their 70s, then gathered electroencephalogram (EEG) readings of brain activity patterns while the participants slept. 

Analyzing the data, the team found that the degree of synchronization of two types of brain waves prominent during sleep—bursts of oscillations called sleep spindles and a slow oscillation or slow wave—correlated to levels of tau protein in the medial temporal lobe, a region of the brain important for memory. More tau buildup was associated with less synchronization of the brain waves. A drop in the amplitude of slow wave was also predictive of higher amounts of amyloid-β in the cortex of the brain. “What was interesting to us was that you could separate the EEG signals,” Winer says, suggesting that the signals and their synchronization could potentially serve as biomarkers of Alzheimer’s disease that may be apparent before more-severe symptoms such as memory loss emerge.

The results are intriguing, says Brendan Lucey, a neuroscientist at Washington University in St. Louis who was not involved in the study. But the team’s claim that the accumulation of tau or amyloid-β generates distinct EEG signals may be a bit premature, he says. “We need a lot more replication and larger samples to see if the differences are true.”

Ashley Yeager is an associate editor at The Scientist. Email her at ayeager@the-scientist.com.