Brain inflammation, while an important aspect of the immune response, plays a negative effect in Alzheimer's disease. Unlike the acute, short-lived inflammation that fights infection, the inflammation associated with Alzheimer's is chronic and persistent. Scientists have been trying to figure out why this happens
Maryland [US], February 16 (ANI): Brain inflammation, while an important aspect of the immune response, plays a negative effect on Alzheimer's disease. Unlike the acute, short-lived inflammation that fights infection, the inflammation associated with Alzheimer's is chronic and persistent. Scientists have been trying to figure out why this happens.
New
research reveals key differences in how the brain's immune system responds to
the disease compared to a bacterial infection. The work is presented at the
69th Biophysical Society Annual Meeting in Los Angeles.
The
study focuses on how immune cells react to amyloid-beta (Ab) plaques, a
hallmark of Alzheimer's, and how this immune response differs from the reaction
to bacterial toxins. "Bacteria cannot enter our brain because of the blood
brain barrier," said Arpan Dey, PhD, a postdoctoral associate in the lab
of Professor David Klenerman at the University of Cambridge in the United
Kingdom. "But small proteins could be acting like bacteria in our brain
and giving rise to neuroinflammation, which could be contributing to
dementia," he added.
Dey
and colleagues used a model system of immune cells and exposed the cells to Ab
aggregates or lipopolysaccharide (LPS), a component of bacterial cell walls
that triggers a strong immune response. They focused on the formation of
structures called myddosomes, which are crucial for initiating inflammation.
The
team discovered that larger Ab clumps trigger more myddosome formation in
immune cells. Smaller Ab clumps, even after longer exposure, failed to trigger
this response. This suggests that the size of the Ab clump is critical for
activating the immune system in Alzheimer's.
In
contrast, LPS triggered a much faster and stronger myddosome response than even
the large Ab aggregates. This difference in timing and intensity may explain
why inflammation in Alzheimer's is chronic and drawn-out, whereas the response
to a bacterial infection is typically more acute and resolves more quickly.
"Our
findings reveal a crucial distinction in how the brain's immune system reacts
to a bacterial infection versus Ab clumps," said Dey. "The slower,
more sustained immune activation by large Ab aggregates may contribute to the
chronic inflammation seen in Alzheimer's disease."
The
team's next step is to start looking at markers of myddosomes in blood samples
from people with dementia and brain samples from the UK Brain Bank.
By understanding the mechanisms driving inflammation in Alzheimer's, they hope to contribute to the development of new therapies that can specifically target the chronic inflammation associated with the disease, potentially slowing its progression.
"This
work opens up new avenues for drug discovery," Dey said, he added,
"by understanding and targeting the pathways involved in the inflammatory
response, we may be able to develop treatments for Alzheimer's and other
neurodegenerative diseases." (ANI)
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