Inflammation may actually protect brains of Alzheimers patients

While most scientists assume that inflammation as a result of disease or injury only adds to the brains woes, researchers at the University of Rochester Medical Center have shown that the opposite may be true for patients with Alzheimers disease.

Washington, June 2 : While most scientists assume that inflammation as a result of disease or injury only adds to the brain's woes, researchers at the University of Rochester Medical Center have shown that the opposite may be true for patients with Alzheimer's disease.

The researchers say that inflammation may instead act as a protector of the brains of Alzheimer's patients by helping them get rid of clumps of material known as amyloid plaques, made up of the peptide amyloid beta, which are a hallmark of the disease.

Published in the Journal of Clinical Investigation, the study suggests that doctors should not rush in to turn off molecular events that are widely considered to be detrimental in people with the disease.

During the study, the researchers had assumed that high levels of IL-1 beta, a signaling molecule that promotes brain inflammation and brings about much of the brain damage after a stroke, might worsen the numbers of amyloid plaques in the mice brains. They, however, observed that it had halved the plaques in the animals.

The new findings attain significance as they may renew efforts to develop a vaccine or other strategies against Alzheimer's by engaging the body's immune system.

"This work provides evidence that blocking all inflammatory responses in Alzheimer's disease is not an ideal therapy. This might hinder processes that are beneficial and part of the body's adaptive response to fight plaques," said Shaftel, a student who conducted the study to earn his doctoral degree as part of the University's Medical Scientist Training (M.D./Ph.D.) Program.

The researchers carried out extensive experiments, and showed that the mice simply were not making fewer plaques, but rather that the body was better at getting rid of the plaques. They suspect the involvement of brain cells called microglia, the major immune cell that rushes to injury sites and helps repair and clean up wounds in the brain.

It is believed that the latest findings may have ramifications for the development of a vaccine or other strategy to protect against or fight off Alzheimer's.

"People have talked for a long time about a balance of 'good guys' and 'bad guys' within the inflammatory process, either causing harm or alleviating the disease. The current work reinforces the idea that inflammation is not simply the bad guy that many people think it is," said O'Banion, another researcher.

"The potential to treat Alzheimer's disease by modulating the immune system is tremendous and is an area that has not been fully explored. That said, people have to remember that the current findings are in mice, not people. We need to be cautious about how to interpret the results," the researcher added.

ANI