Inflammation in the brain may not be so bad after all when it comes to Alzheimers disease.
In the June 1 issue of the Journal of Clinical Investigation, a team of scientists from the University of Rochester Medical Center shows that a key inflammatory regulator, a known villain when it comes to parsing out damage after a stroke and other brain injuries, seems to do the opposite in Alzheimers disease, protecting the brain and helping get rid of clumps of material known as plaques that are a hallmark of the disease.
While many scientists have assumed that inflammation as a result of disease or injury only adds to the brains woes, the new findings show that the opposite may be true when it comes to Alzheimers disease. Perhaps inflammation is playing the role of protector and is acting more like an ambulance crew helping at the site of a road wreck, not causing the crash.
The work suggests that doctors not rush in to turn off molecular events that scientists have widely considered to be detrimental in people with the disease. The findings could also renew efforts to develop a vaccine or other strategies against Alzheimers by engaging the bodys immune system.
The team expected to see the telltale clumps of material known as amyloid plaques, made up of the peptide amyloid beta, worsen. Instead, to the teams surprise, the brains of the mice with IL-1beta stuck in overdrive had only about half
This work provides evidence that blocking all inflammatory responses in Alzheimers disease is not an ideal therapy, added Shaftel. This might hinder processes that are beneficial and part of the bodys adaptive response to fight plaques.
The new findings hinge on a very special mouse that Shaftel spent three years creating with the guidance of his adviser, M. Kerry OBanion, M.D., Ph.D., associate professor of Neurobiology and Anatomy. Shaftel genetically engineered a one-of-a-kind mouse that gives him pinpoint control over bra
Contact: Tom Rickey
University of Rochester Medical Center