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.
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 trigger production of the NLRP3 inflammasome. Therefore, these mice were no longer able to synthesize the protein complex. As a result, the animals developed only relatively mild symptoms of the disease. Moreover, their brains showed only reduced amounts of the damaging plaques.