Excessive activity of microglia, the immune cells of the central nervous system, may serve as a key driver of sleep loss in Alzheimer’s disease, and this sleep disruption occurs independently of the amount of amyloid plaques. The findings, reported by Science Daily, reshape the understanding of the disease’s underlying mechanisms.
Researchers compared mice genetically predisposed to forming amyloid plaques with healthy animals. They discovered that even at an early stage, the pathology selectively reduces slow-wave sleep, and by 18 months, the impairment did not worsen despite plaque levels more than doubling. This led the scientists to suspect that an initial immune response alone might be sufficient to sustain a persistent sleep deficit.
To test this hypothesis, mice were given a drug for two weeks that temporarily eliminated about 87% of microglia. Following treatment, the animals began sleeping more than two additional hours per day, while the volume of amyloid deposits remained unchanged.
Researchers are now exploring ways to reduce the overactivity of these cells without completely removing them. In the future, portable EEG systems could help detect characteristic sleep changes in the early stages of the disease. However, since this study was conducted on animals, its findings cannot yet be directly applied to humans.
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