Researchers at the University of Kentucky say they have identified a damaging process in Alzheimer’s disease that may help explain why sleep problems occur. According to ScienceDaily, the study found that microglia — the brain’s resident immune cells — were the main drivers of sleep loss in an animal model of the disease.
In the study, which was published in the journal Alzheimer’s & Dementia, scientists led by Shannon L. Macauley and first author Nicholas J. Constantino tested mice with a genetic tendency to develop amyloid plaques. They compared those animals with normally aging mice at both six months and 18 months of age, using EEG and EMG monitoring to track sleep and brain activity.
The researchers also used light sheet microscopy to map plaque buildup and immune cells throughout the brain. To see whether microglia were responsible for the sleep disruption, the team used the drug Pexidartinib, also known as PLX3397, which temporarily removed about 87% of the brain’s immune cells after 14 days of treatment.
When the microglia were depleted, the mice gained more than two hours of sleep each day. The findings suggest that sleep loss in Alzheimer’s may be driven by an immune response to plaques rather than by plaques alone or by damaged neurons, according to the researchers.
The study also found that amyloid pathology mainly reduced nonrapid eye movement, or NREM, sleep, while normal aging primarily affected REM sleep. Researchers said the results point to a possible new treatment target and described the work as paradigm shifting.
