Researchers have discovered new details about Alzheimer's disease, revealing how it transforms from a protector into an adversary.

Inflammation serves as a natural protective mechanism of the body that swiftly addresses injuries or infections. However, in Alzheimer's disease, this protective response becomes chronic, potentially exacerbating its progression. A recent study explains why the brain's immune system reacts differently to Alzheimer's compared to bacterial infections, reports Newswise.

At the upcoming 69th annual meeting of the Biophysical Society in Los Angeles, Dr. Arpan Day, a postdoctoral researcher in Professor David Klenerman's lab at the University of Cambridge, will present findings on inflammation and Alzheimer's disease. His research investigates the immune cells' response to amyloid-beta (Aβ) plaques—a hallmark of Alzheimer's—and compares it to their reaction to bacterial toxins.

Dr. Day notes that while the blood-brain barrier prevents bacteria from entering the brain, small proteins like Aβ can mimic bacterial effects, potentially leading to neuroinflammation and contributing to the development of dementia. The research team exposed immune cells to Aβ aggregates and lipopolysaccharide (LPS), a component of bacterial cell walls that triggers a strong immune response.

The scientists focused on the formation of mitochondria—structures necessary for initiating inflammation. Their observations revealed that larger Aβ aggregates induced the formation of mitochondria in immune cells, whereas smaller Aβ aggregates did not elicit such a response even after prolonged exposure. This suggests that size is critical for activating the immune system in Alzheimer's disease.

In contrast, LPS triggered a quicker and more robust mitochondrial response than large Aβ aggregates. This difference in timing and intensity of the response may explain why inflammation in Alzheimer's disease is prolonged, while the immune reaction to bacterial infections is generally rapid and resolves quickly. Dr. Day emphasizes that understanding these differences in immune activation could be key to developing therapies aimed at chronic inflammation associated with Alzheimer's disease.

The researchers plan to investigate markers of mitochondrial formation in blood samples from individuals with dementia and brain samples from the UK Brain Bank. By delving into the mechanisms that trigger inflammation in Alzheimer's, they hope to contribute to the development of treatments aimed at alleviating chronic inflammatory responses and potentially slowing disease progression.

This study not only deepens scientists' and clinicians' understanding of the pathology of Alzheimer's disease but also opens new avenues for drug discovery. By targeting pathways involved in the brain's immune response to Aβ aggregates, it may be possible to develop therapies aimed at reducing chronic inflammation, offering hope to those suffering from Alzheimer's and other neurodegenerative diseases, researchers believe.

Important! This article is based on the latest scientific and medical research and does not contradict them. The text is for informational purposes only and does not contain medical advice. For diagnosis, please consult a physician.