Nighttime light tied to sleep disruption in Alzheimer’s mouse studies

Dim light at night and inflammation in the brain may help disturb sleep and daily body rhythms in Alzheimer’s disease models, according to two new studies from University of Kentucky researchers. The findings matter because sleep problems are common in Alzheimer’s disease and may appear before severe memory symptoms, the researchers said.

The work, led by investigators at the university’s Sanders-Brown Center on Aging, examined two related questions: whether everyday nighttime light can affect Alzheimer’s-linked brain changes, and whether neuroinflammation can drive poor sleep after disease-related pathology is already present.

One study, published in SLEEP, tested dim nighttime light comparable to exposure from televisions, phones, hall lights or streetlights, according to the University of Kentucky. In Alzheimer’s disease models, the researchers reported that the light disrupted daily activity rhythms, made those rhythms less stable and increased fragmentation.

The same study found that dim light at night modestly increased amyloid buildup in the disease models and shifted microglial activity toward a more immune-activated state, according to the research team. Microglia are immune-related cells in the brain that have been studied for their role in Alzheimer’s disease processes.

Adam Bachstetter, an associate professor of neuroscience in the University of Kentucky College of Medicine and lead author of the study, said the research examines why sleep and biological rhythms break down in Alzheimer’s disease and whether those changes are shaped by both external conditions and inflammation inside the brain.

An editorial published with the SLEEP paper described artificial light at night as a potentially changeable environmental factor that could affect Alzheimer’s disease risk or progression through circadian and neuroimmune pathways, according to the journal summary cited by the university.

A second study, published in Alzheimer’s & Dementia, looked at what may cause sleep problems once Alzheimer’s-related pathology is present. The researchers tracked sleep, activity rhythms, cognition and inflammatory signaling over time in Alzheimer’s disease models, according to the University of Kentucky.

That study found that sleep disruption and more fragmented circadian rhythms developed in midlife before major memory deficits appeared, the researchers reported. The team then tested MW151, a compound developed by Sanders-Brown director Linda Van Eldik that targets excessive inflammatory signaling from glial cells in the brain.

MW151 improved sleep patterns and helped restore more typical daily rhythms without lowering amyloid buildup, according to the study. Bachstetter said that result separates sleep disruption from amyloid load and points to neuroinflammatory signaling as a modifiable contributor to poor sleep in Alzheimer’s-related pathology.

The University of Kentucky researchers said the studies add to evidence that sleep and circadian health may be part of brain aging, rather than only late-stage symptoms of disease. Bachstetter said poor sleep may interact with amyloid pathology, microglial function and inflammation in ways that influence disease progression.

The findings remain preclinical and do not directly create medical guidance for people, according to the researchers. Marilyn Duncan, a professor of neuroscience in the University of Kentucky College of Arts and Sciences and a co-author, said reducing unnecessary nighttime light, keeping a consistent sleep schedule and supporting healthy circadian rhythms are low-risk steps that match current sleep health guidance.

The studies involved University of Kentucky researchers and trainees across neuroscience, biology, biomedical engineering, molecular and cellular biochemistry, and the Spinal Cord and Brain Injury Research Center, according to the university.

This story draws on original reporting from Medical Xpress.