New research has shown that a well-known inflammatory process could play a role in the progression of Alzheimer’s Disease. The discovery could lead to new research on a different way to combat the disease.

“This finding represents an important new clinical target for patients with Alzheimer’s disease,” said Dr. Douglas Golenbock, chief of infectious diseases and immunology at the University of Massachusetts Medical School. “We’ve known for years that the plaques associated with Alzheimer’s were surrounded by microglia, the resident immune cell of the central nervous system. What we didn’t know was what role, if any, inflammation played in the progression of the disease. With this link we have a new path to potentially identifying and attacking this horrible disease.”

Golenbock and his fellow researchers found in previous studies that neurons in cultures die when the brain’s immune defense is exposed to beta amyloids. Beta amyloid peptides aggregate into plaques in the brains of Alzheimer’s patients and are believed to be the main cause of neuron death.

Inflammation in the brain can occur when amyloids spur microglia into making neurotoxic compounds. Golenbock deciphered the mechanism at play, showing how amyloids activate a multi-protein receptor complex, known as NLRP3 inflammasome, which leads to the production of interleukin-1 beta (IL-1B), a pro-inflammatory cytokine.

The new research has been published in the journal Nature. The technical description above means that new mechanisms have been identified as playing a part in Alzheimers. Attacking these mechanisms could represent a novel way of battling Alzheimer’s. For example, drugs that attack IL-1b already exist, and were created for rheumatoid arthritis patients.

“These findings suggest that a knockout of NLRP3…or mature IL-1B may represent a novel therapeutic intervention for Alzheimer’s disease,” said Golenbock. “It’s possible that drugs that block NLRP3 or IL-1B – including some of which are already in clinical trials or on the market – might provide some benefit.

“The critical part, though, is how much NLRP3 or IL-1B production can these drugs disrupt. I believe that it’s not enough to block just 90 percent; it will probably have to be closer to 100 percent.”