Researchers from the German Center for Neurodegenerative Diseases (DZNE) and the University of Bonn have discovered that the protein complex NLRP3 is a critical factor in the development of Alzheimers disease.

They studied the complex “NLRP3 inflammasome”, which has a very important role in the immune system. When it is activated, immune cells are mobilized and substances that cause inflammation are released.

Several studies over the last few years have focused on how the body’s immune response raises Alzheimer’s risk and how certain genes are involved. Another study found that a genetic mutation in the TREM2 gene, which triggers immune system responses, is also linked to Alzheimer’s risk.

With Alzheimer’s disease, once the sensor is activated, it causes nerve cells to die off, which results in a loss of brain function and cognitive ability.

Alzheimer’s disease occurs when plaques start forming in the brain, these plaques activate the NLRP3 inflammasome. The researchers looked at the effect that increased activity of the inflammasome has on the brain.

Prof. Michael Heneka and his team studied the brains of dead Alzheimer’s patients and mice with disorders related to Alzheimer’s disease. They found that the NLRP3 inflammasome was active in both the humans and mice.

The researchers believed that by suppressing the inflammatory reactions of the protein complex there would be a reduction of damaging plaques. They removed the genes that activate NLRP3 inflammasome activity in a group of mice with disorders associated with Alzheimer’s.

After removing the gene from the mice, they were no longer able to synthesize the protein complex. This resulted in only mild symptoms of the disease showing.

This is promising news and could result in pharmaceuticals being able to target the protein complex and inhibit it’s activity.

Prof. Heneka said:

“We have stumbled upon a critical factor in the development process of Alzheimer’s. Given these findings it appears to be a very promising possibility to block the activity of the inflammasome. At present various options are being pursued to act upon the course of the disease,” says the neuroscientist. “Our results points to a new possibility. Nevertheless, we are still in the process of doing basic research.”

The team are already searching for possible ways to block the inflammasome. Heneka added: “The testing of potential substances in the laboratory would be a next step. We hope to start as early as next year.”

Written by Joseph Nordqvist