Researchers at the University of Kentucky investigated why Alzheimer’s-related changes disrupt sleep, focusing on microglia, the brain’s immune cells. In mice engineered to develop amyloid plaques, they compared sleep and brain activity at early and advanced stages of pathology, using EEG and muscle recordings to track sleep stages and imaging to map plaques and microglia. Sleep disruption appeared early and did not worsen as plaque levels more than doubled. Unlike normal aging, which mainly reduced REM sleep, Alzheimer’s-like pathology selectively impaired NREM sleep, including deep, restorative sleep.
To test whether microglia contributed to the problem, the team gave the mice pexidartinib for 14 days, temporarily depleting about 87% of their microglia. The mice then slept more than two additional hours per day and had longer periods of NREM sleep, despite no reduction in amyloid plaques. The findings suggest that inflammation triggered by microglia, rather than plaques alone, can drive sleep loss and may offer a treatment target distinct from plaque removal. The experiment does not establish a treatment for people: it was conducted in mice, and eliminating most brain immune cells is not a practical therapy. Researchers hope to find ways to regulate microglial activity without removing the cells.
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