Brain inflammation, while a crucial part of the body’s immune response plays an adverse role in Alzheimer’s disease. In contrast to the acute, short -term inflammation that fights infection, the inflammation is associated with Alzheimer’s chronic and persistent. Scientists have tried to understand why this is happening.
New research reveals important differences in how the brain’s immune system reacts to the disease compared to a bacterial infection. The work will be presented at the annual meeting of the 69th Biophysical Society, which will be held on 15 – 19 February 2025 in Los Angeles.
The study focuses on how immune cells react to amyloid-beta (Aβ) plaques, a characteristic of Alzheimer’s, and how this immune response differs from the reaction to bacterial toxins. “Bacteria cannot get into our brains because of the blood -brain barrier,” said Arpan Dey, PhD, a post -doctoral employee in the lab of Professor David Klennerman at the University of Cambridge in the United Kingdom. “But small proteins can behave like bacteria in our brains and give rise to neuro inflammation, which could contribute to dementia,” he added.
Dey and colleagues used a model system of immune cells and exposed the cells to AP -aggregates or lipopolysaccharide (LPS), a component of bacterial cell walls that cause a strong immune response. They focused on the formation of structures called Myddosomes, which are crucial for initiating inflammation.
The team discovered that larger AP clonts activate more myddosome formation in immune cells. Smaller AP clumps, even after longer exposure, could not initiate this reaction. This suggests that the size of the AP cubes is crucial for activating the immune system in Alzheimer’s.
LPS, on the other hand, has caused LPS a much faster and stronger myddosome response than even the large AP aggregates. This difference in timing and intensity can explain why inflammation in Alzheimer’s is chronic and postponed, while the reaction to a bacterial infection is usually acuter and dissolves faster.
Our findings reveal a crucial distinction in how the brain’s immune system reacts to a bacterial infection versus Aβ clonts. The slower, more persistent immuneactivation by large AP -aggregates can contribute to the chronic inflammation that is seen in Alzheimer’s disease. “
Arpan Dey, PhD
The next step of the team is to look at myddosomes in blood samples of people with dementia and brain samples of the British brain bank.
By understanding the mechanisms that stimulate inflammation in Alzheimer’s, they hope to contribute to the development of new therapies that focus specifically on the chronic inflammation that is accompanied by the disease, which may be delayed.
“This work opens new ways for discovering medicines,” said Dey, he added, “by understanding and focusing the paths involved in the inflammatory response, we may develop treatments for Alzheimer’s and other neurodegenerative diseases.”