When Adam Bachstetter first noticed how everyday light—the glow of a hallway nightlight, the flicker of a sleeping TV—might quietly shape brain health decades later, he wasn't looking for good news. He was looking for answers. What he found points toward something unexpected: that the nightlight you leave on for comfort might matter more than anyone realized.
Bachstetter, an associate professor of neuroscience at the University of Kentucky, leads research at the Sanders-Brown Center on Aging in Lexington that's revealing how environmental factors and brain inflammation interact in ways that could influence Alzheimer's disease. In two recently published studies, his team discovered that dim light exposure at night—similar to the ambient glow from common household sources—disrupted daily activity rhythms, reduced rhythm stability, and in Alzheimer’s disease models, modestly worsened amyloid buildup while shifting immune cells in the brain toward a more activated state.
"These studies examine why sleep and daily biological rhythms become disrupted in Alzheimer’s disease, and whether those disruptions are influenced by both the outside environment and inflammation inside the brain," Bachstetter said.
But the research isn't just identifying problems. It may have found a solution.
In the second study, published in Alzheimer's & Dementia, researchers tracked sleep patterns, activity rhythms, cognition, and inflammatory signaling over time in Alzheimer’s disease models. They noticed something striking: disrupted sleep and fragmented circadian rhythms emerged in midlife, before major memory deficits ever appeared. The team then tested a compound called MW151, developed by Sanders-Brown director Linda Van Eldik, which targets excessive inflammatory signaling from glial cells in the brain. The results were striking: treatment with MW151 improved sleep patterns and restored more typical daily rhythms without reducing amyloid buildup.
The implications are significant. "We now know that sleep can be improved without reducing amyloid," Bachstetter said. "This finding separates sleep disruption from amyloid load and points to neuroinflammatory signaling as a modifiable driver of poor sleep in Alzheimer’s-related pathology."
The work is still preclinical and doesn’t yet translate directly into clinical recommendations. But co-author Marilyn Duncan, a professor of neuroscience at Kentucky, says the findings reinforce what sleep health guidance already suggests—and point toward future possibilities. "Practical steps such as reducing unnecessary light exposure at night, keeping a consistent sleep schedule and supporting healthy circadian rhythms are low-risk strategies that align with current sleep health guidance," she said.
For millions concerned about brain health, the research offers a quiet reminder: the choices people make tonight—in how they dim their screens, whether they draw their curtains, when they turn off the lights—might matter more than anyone knew. And for scientists, the door is now open to explore whether addressing neuroinflammation could one day help people sleep better, think more clearly, and age with greater resilience.