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Scientists have identified an unexpected mechanism underlying sleep disruption in Alzheimer’s disease: hyperactive immune cells within the brain itself. The findings suggest that inflammation triggered by microglia, rather than amyloid plaques alone, bears primary responsibility for the severe sleep disturbances that afflict Alzheimer’s patients.
In laboratory studies using mice engineered to develop amyloid plaques, researchers observed that overactive microglia generated inflammatory responses that prevented the brain from achieving adequate deep sleep. When investigators temporarily depleted most of these immune cells, study subjects regained more than two hours of daily sleep despite the persistence of amyloid accumulation in brain tissue.
The discovery marks a significant departure from conventional understanding of Alzheimer’s pathology, which has long centered on amyloid and tau proteins as primary disease drivers. By demonstrating that microglial activation independently disrupts sleep architecture, the research opens new therapeutic avenues that may bypass the need to eliminate plaques entirely.
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