Researchers have identified what may be an unexpected cause of the severe sleep problems that affect many people with Alzheimer’s disease.
Their study suggests that overactive immune cells, rather than protein plaques alone, may be keeping the brain awake.
Sleep problems are one of the earliest and most common symptoms of Alzheimer’s disease. Many people begin sleeping poorly years before serious memory loss appears. Scientists have long believed these changes were mainly caused by damage to brain cells or the buildup of amyloid plaques.
Amyloid plaques are sticky clumps of protein that collect between brain cells. They are considered one of the main features of Alzheimer’s disease. However, researchers have wondered whether the plaques themselves are responsible for sleep problems or whether another process is involved.
A team from the University of Kentucky explored this question using mice that develop Alzheimer’s-like brain changes. Their findings, published in Alzheimer’s & Dementia, suggest that immune cells in the brain, called microglia, may be the real cause of much of the sleep disruption.
Microglia normally protect the brain by removing waste and responding to injury. But when they react to amyloid plaques, they can trigger inflammation. The researchers believe this immune response may keep the brain in an overactive state instead of allowing it to rest.
The scientists monitored the animals using EEG recordings, which measure electrical activity in the brain, together with muscle activity recordings that helped identify different sleep stages. They also used advanced imaging to observe both amyloid plaques and immune cells throughout the brain.
To test whether microglia were responsible, the researchers temporarily removed most of these immune cells using an existing drug. After two weeks, about 87 percent of the microglia had disappeared.
The results surprised the team. Mice with Alzheimer’s-related changes gained more than two extra hours of sleep each day. Their deep restorative sleep also improved, even though the amount of amyloid plaque remained unchanged.
The study found that sleep loss began early, when plaques first appeared, and did not become much worse even after plaque levels more than doubled. This suggests the first wave of immune activity may trigger lasting sleep problems that continue throughout the disease.
The researchers also found differences between normal aging and Alzheimer’s disease. Normal aging mainly reduced dreaming sleep, while Alzheimer’s mainly reduced deep sleep, the stage that helps the brain repair itself, store memories, and remove waste products.
The team believes the findings could eventually lead to new treatments that calm overactive microglia instead of directly targeting amyloid plaques. They are already investigating medicines such as metformin and stiripentol to see whether they can safely reduce harmful immune activity without removing the cells completely.
The researchers also hope portable EEG devices may one day help detect Alzheimer’s-related brain changes earlier and more easily. Such tools could allow doctors to monitor people at home and identify warning signs before major symptoms develop.
The study provides strong evidence that inflammation caused by brain immune cells may play a much larger role in Alzheimer’s disease than previously thought. However, the work was carried out in mice, so researchers must confirm whether the same process occurs in people.
If future human studies support these findings, reducing harmful immune activity while restoring healthy sleep could become an important new strategy for slowing Alzheimer’s disease and improving patients’ quality of life.
This research offers a fresh way of thinking about Alzheimer’s disease by showing that inflammation may be just as important as protein buildup. The study is strengthened by detailed brain recordings and imaging, but it remains an animal study.
Future research will need to determine whether calming overactive immune cells can safely improve sleep, thinking, and daily life for people living with Alzheimer’s.
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