Sleep Brainwaves Could Reveal Early Signs of Alzheimer’s and Multiple Sclerosis

Scientists have found that damaged myelin sheaths lead to abnormal rhythms in brainwave activity during sleep. These findings could have major implications for the development of biomarkers and therapies for neurodegenerative diseases that affect myelin, such as multiple sclerosis (MS) or Alzheimer’s disease. 

“The myelin sheath helps electrical signals travel efficiently through brain circuits,” said Mohit Dubey, PhD, senior scientist at the Netherlands Institute for Neuroscience, who presented the study at the Federation of European Neuroscience Societies (FENS) Forum 2026. “We wanted to understand whether myelin damage could also affect how brain circuits behave during sleep. By studying this link, we hope to better understand what causes sleep disturbances in neurological disease and whether sleep-related brain signals could serve as biomarkers for diseases that are yet to show clinical symptoms, as well as showing disease progression.”

Although sleep is known to play a key role in brain health, its study has often been overlooked in the context of neurodegenerative diseases. In conditions like Alzheimer’s, sleep disruptions are known to contribute to fatigue and cognitive decline, especially during the REM sleep phase, which is critical to preserve healthy cognition and memory.

“Sleep disturbances are extremely common in neurological diseases such as multiple sclerosis and Alzheimer’s disease, but the biological reasons for these problems remain poorly understood,” said Dubey. “Understanding the biological link between sleep and brain circuit dysfunction could help guide future strategies for improving sleep and brain health in these conditions.”

Dubey’s team had previously shown that loss of myelin sheaths cause abnormal spikes of brainwave activity in the brain during sleep that seemed to resemble those observed in epilepsy and Alzheimer’s. In the current study, the researchers compared electroencephalogram (EEG) recordings of MS patients during sleep with mouse models of damaged myelin and Alzheimer’s. In both humans and mice, myelin loss resulted in similar abnormal bursts of brain activity during non-REM sleep phases and slower brainwave rhythms during REM sleep. 

“REM is a stage of sleep associated with dreaming and replay of daytime experiences. In this state the brain produces rhythmic electrical patterns called oscillations that help coordinate communication between neurons,” said Dubey. “Our findings show that these rhythms become disrupted and slower when myelin degenerates, and that the electrical spikes seen during sleep are closely linked to the stability of brain circuits affected by neurodegenerative diseases such as MS and Alzheimer’s.” 

While there are no treatments that can repair damaged myelin, some MS drugs are able to slow down the immune system’s attack on myelin sheath to reduce or halt disease progression. Further research to determine how exactly myelin damage alters brainwave patterns during sleep could aid the early detection of myelin degeneration and inform the design of therapeutic approaches that target myelination. 

“This opens new research directions exploring how sleep rhythms depend upon the myelination status of the brain circuits,” said Dubey. “Sleep recordings may provide a non-invasive way to detect early changes in brain circuit myelination in neurological disease. This could eventually help clinicians monitor disease progression, and we want to investigate whether sleep recordings could be used as biomarkers to detect early changes in brain circuit function.”

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