Maryland [US]: Chronic brain inflammation plays a crucial role in Alzheimer’s disease, differing significantly from the short-term immune response seen in bacterial infections, according to new research presented at the 69th Biophysical Society Annual Meeting in Los Angeles.
The study, led by Dr. Arpan Dey, a postdoctoral associate in Professor David Klenerman’s lab at the University of Cambridge, examines how the brain’s immune system reacts to amyloid-beta (Ab) plaques—one of the hallmarks of Alzheimer’s. Researchers found that while bacterial infections trigger an acute and temporary immune response, the inflammation in Alzheimer’s disease is persistent and prolonged.
Alzheimer’s vs. Bacterial Infections: How the Immune System Reacts
Dr. Dey and his team used a model system of immune cells exposed to either amyloid-beta (Ab) aggregates or lipopolysaccharide (LPS), a bacterial toxin known to trigger a strong immune response. They specifically analyzed the formation of myddosomes—molecular structures essential for initiating inflammation.
Their findings revealed:
- Larger Ab clumps trigger more myddosome formation, while smaller Ab aggregates fail to do so, even with prolonged exposure.
- LPS causes a much faster and stronger immune response compared to Ab clumps, leading to a rapid resolution of inflammation in bacterial infections.
- The slower, sustained activation by Ab aggregates may be a key factor in the chronic inflammation associated with Alzheimer’s disease.
“Bacteria cannot enter our brain because of the blood-brain barrier,” Dr. Dey explained. “But small proteins could be acting like bacteria in our brain and giving rise to neuroinflammation, which could be contributing to dementia.”
New Avenues for Alzheimer’s Treatment
The next phase of research will involve analyzing blood samples from individuals with dementia and brain tissue from the UK Brain Bank to identify myddosome markers.
By pinpointing the mechanisms driving chronic inflammation in Alzheimer’s, researchers hope to develop targeted therapies that slow disease progression.
“This work opens up new avenues for drug discovery,” said Dr. Dey. “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.”
This breakthrough study highlights the critical role of immune system dysfunction in Alzheimer’s and offers promising insights for future treatments.