The inflammation of the brain, while an important aspect of the immune response, negatively affects Alzheimer’s disease. Unlike acute, short -term inflammation that fights infection, the inflammation associated with Alzheimer’s is chronic and frequent. Scientists are trying to find out why this happens.
New research suggests how the brain’s immune system responds to the disease than a bacterial infection. This work is presented at the 69th Biofigical Society annual meeting at Los Angeles.
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How the immune system reacts
The study focuses on how immune cells react to a hallmark of amyloid-beeta (AB) plaques, Alzheimer’s, and this immune response varies from the reaction of bacteria toxins of bacteria. “Bacteria cannot enter our brain due to the brain barrier,” said a postdotoral Associate Arpan Dey at the laboratory of Professor David Clainman at Cambridge University at the United Kingdom. “But small proteins can act like bacteria in our brain and give rise to neuroinphone, which can contribute to dementia,” he said.
Dey and colleagues used a model system of immune cells and exposed cells to ab agargeates or lipopolsacharides (LPS), a component of bacterial cell walls that trigger a strong immune response. He focused on the formation of structures called Myddosomes, which are important to begin inflammation.
The team found that large AB clamps trigger more myddosome formation in immune cells. Small AB clump, even after prolonged risk, failed to trigger this reaction. This suggests that the size of the AB clump is important to activate the immune system in Alzheimer’s.
In contrast, LPS triggers much faster and stronger myddosome reaction than the large AB set. This difference in time and intensity can explain why the swelling in the Alzheimer’s is chronic and drawn, while a bacterial infection usually is more intense and is more rapidly resolved.
“Our findings show how the brain’s immune system reacts to a bacterial infection vs. AB clumps, revealing a significant difference,” Dey said. “Slow, more constant immune activation by large AB sets can contribute to chronic inflammation seen in Alzheimer’s disease.”
The next step of the team is to start looking at the markers of myddosomes in blood samples from people with dementia and brain samples from the UK Brain Bank.
By understanding the mechanisms running inflammation in the Alzheimer’s, they expect to contribute to the development of new remedies that can target chronic inflammation particularly to the disease, possibly slowing its progression.
“This task opens new avenues for the discovery of drugs,” Dey said, he said, “By understanding and targeting the routes involved in the inflammatory reaction, we may be able to develop treatment for Alzheimer’s and other neurodynative diseases. “
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