Alzheimer’s disease is associated with the deposition of a protein called amyloid-beta in the brain. The aggregation of this protein gives rise to a chain of events, that ultimately harm neurons and lead to their loss. “Alzheimer’s disease involves a complex interaction of different mechanisms. One of these is neuroinflammation. That’s what we looked at in our studies. Specifically, we pharmacologically manipulated a molecular complex called the NLRP3 inflammasome. It is found in microglia, which are the immune cells of the brain,” says ImmunoSensation2 member Dr. Róisín McManus, research group leader at the Bonn DZNE and investigator at UKB’s Institute of Innate Immunity.
Previously unknown pathways
The NLRP3 inflammasome is like a control switch: In Alzheimer’s disease, its activation triggers an inflammatory response that harms neurons. For this reason, researchers have been exploring ways to inactivate the NLRP3 inflammasome using drugs. The current results support this approach. “It is known that inhibiting NLRP3 not only reduces neuroinflammation, but also helps microglia clear the harmful amyloid-beta deposits, a process called phagocytosis. The novelty of our findings is that they provide...