The Bonn site of the German Center for Neurodegenerative Diseases (DZNE) and the University of Bonn are leading contributors.
The complex named "NLRP3 inflammasome" is composed of several proteins and plays a key role in the immune system. It resembles a fire alarm sensor that triggers a chain reaction when activated. As a result, immune cells are mobilized and substances that foster inflammation are released. This process can be triggered by infections, which are subsequently suppressed by the immune response. However, in the case of Alzheimer's disease, the activation of the molecular alarm may have negative consequences: nerve cells are damaged and die. Ultimately, this leads to the loss of brain function and mental capabilities in humans.
Alzheimer's disease is accompanied with deposits in the brain. That these so-called "plaques" have the capability to activate the NLRP3 inflammasome had already been identified by investigating individual cells. But the exact effect on the organism was unknown. "It was unclear what consequences an increased activity of the NLRP3 inflammasome could have on the brain," explains Prof. Michael Heneka, who conducts research at both, the DZNE and the University of Bonn. Working in a team with immune researcher Eicke Latz as well as with other colleagues, Heneka has now been able to show that the protein complex does in fact play a determining role in the development of Alzheimer's disease.
Studies involved humans and mice
The researchers collected a comprehensive chain of evidences: they examined both the brains of deceased Alzheimer patients and of mice who exhibited behavioural disorders that are typically associated with Alzheimer's disease. The researchers found an activated form of the NLRP3 inflammasome in both cases.
Looking at another group of mice, the scientists examined possibilities for suppressing inflammatory reactions. To achieve this, they removed the genes that
|Contact: Dirk Frger|
Helmholtz Association of German Research Centres