Health
New research sheds light on brain inflammation in Alzheimer's disease
brain inflammationan important part of the body's immune response plays a detrimental role in Alzheimer's disease. Unlike acute, short-lived inflammation that fights infection, inflammation associated with Alzheimer's disease can be chronic and persistent. Scientists are trying to understand why this happens.
New research reveals important differences in how the brain's immune system responds to disease compared to bacterial infections. This work will be presented at the 69th Annual Meeting of the Biophysical Society, held in Los Angeles from February 15th to 19th, 2025.
This study focuses on immune cells' responses to amyloid beta (Aβ) plaque, a characteristic of Alzheimer's disease, and how this immune response differs from that to bacterial toxins. “Bacteria cannot enter the brain due to brain barriers,” said Dr. Alpan Dei, a postdoctoral associate in Professor David Krenerman's lab at the University of Cambridge, UK. “But small proteins act like bacteria in our brains, which can cause neuroinflammation, which can contribute to dementia,” he added.
Dey and colleagues used a model system of immune cells to expose cells to Aβ aggregates or lipopolysaccharides (LPS). This is a component of the bacterial cell wall that causes a strong immune response. They focused on the formation of a structure called Myddosomes, which is important to initiating inflammation.
The team discovered that larger Aβ clamps cause more midosome formation in immune cells. Smaller Aβ masses were unable to induce this reaction even after long exposure. This suggests that the size of the Aβ mass is important for activating the immune system in Alzheimer's disease.
In contrast, LPS triggered a stronger myDosome response at much faster and faster than larger Aβ aggregates. This difference in timing and intensity may explain why the inflammation in Alzheimer's disease is chronically elicits, but the response to bacterial infections is usually more severe and resolves faster.
Our findings reveal important distinctions about how the brain's immune system responds to bacterial infections to masses of Aβ. Slower, more sustained immune activation by large Aβ aggregates may contribute to the chronic inflammation seen in Alzheimer's disease. ”
Dey Arpan, PhD
The next step for the team is to start looking at midsome markers in blood samples of people with dementia and brain samples from the UK brain bank.
By understanding the mechanisms that promote inflammation in Alzheimer's disease, they want to contribute to the development of new therapies that may specifically target disease-related chronic inflammation, which progresses slowly. It may be.
“This work opens a new pathway for drug discovery,” Dey added.
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