Scientists identify brain inflammation prevention as key to Alzheimer’s treatment

Scientists from Dzne, University Hospital Bonn (UKB) and the University of Bonn provide new proof that preventing brain inflammation is a promising approach for the treatment of Alzheimer’s disease. Their findings, based on studies in cell culture, mice and tissue samples of patients, can contribute to the development of more effective therapies. They are published in the scientific journal Immunity.

Alzheimer’s disease, the most common form of dementia, is associated with the deposit of proteins in the brain. The aggregation of these proteins, known as “amyloid-beta”, give rise to a series of events that ultimately harm neurons and lead to their loss.

Alzheimer’s disease includes a complex interaction of different mechanisms. One of these is neuro inflammation. That is what we looked at in our studies. In particular, we manipulated a molecular complex called the NLRP3 inflammation pharmacologically. It is found in microglia, the immune cells of the brain. “

Dr. Róisín McManus, leader of Dzne Research Group, researcher at UKB’s Institute of Institute or Institute or Member of the “ImmunoSensation2” Cluster of Excellence, University of Bonn

Previously unknown paths

The “NLRP3 -inflammasome” is as a control switch: in Alzheimer’s disease, the activation of it causes an inflammatory response that damages neurons. For this reason, researchers have investigated ways to inactivate this molecular complex with the help of medicines. The current results support this approach. “It is known that the braking of NLRP3 not only reduces neuro inflammation, but also microglia helps to erase the harmful amyloid-beta deposits, a process called phagocytosis. The novelty of our findings is that they offer a better understanding of The important role that NLRP3 plays in Microglia and we also unravel the mechanism behind why its inhibition is so useful, “says McManus. “In our studies we have identified unknown signal routes that have been influenced by NLRP3. In particular, we have established that NLRP3 regulates how microglia uses nutrients and how these work on genes that have a major impact on the function of microglia. This is very relevant For their ability to perform phagocytosis these findings can help with the development of therapies for dementia.

International business

In this project, the Bonn-based researchers collaborated with the Luxembourg Center for Systems Biomedicine, University of California San Diego, Technical Universität Braunschweig, Novartis Switzerland and other institutions in Europe and beyond.