A recent study co-authored by Harvard Medical School Professor Rudolph E. Tanzi has found that a protein once believed to have no other function except playing a key role in Alzheimer’s disease may actually be beneficial to the immune system.

Tanzi and colleagues discovered similarities in function between the Alzheimer’s disease-related protein beta-amyloid, or A-beta, and LL-37, a well-known protein found in the first line of defense in the immune system.

“This finding gives us a strong inkling of what [A-beta] is doing and can provide us with some clues, not only about the origin of the disease, but also how to think about it therapeutically,” said Lee E. Goldstein, one of the study’s co-authors and a professor at the Boston University School of Medicine. “It’s likely that A-beta plays an important protective role in our health, in addition to being what was once considered a ‘bad peptide.’”

In some cases, researchers found that A-beta was more effective as an anti-microbial protein than LL-37. But Medical School professor and study co-author Robert D. Moir said that researchers need to now focus on making sure the findings on the beneficial function of A-beta apply to actual people.

“This study was done in a test tube,” Moir said. “We have to show in vivo that it does in fact work.”

Moir added that the laboratory was now examining the relationship between A-beta levels in live animals and their susceptibility to infections. The study’s researchers said they believe that their surprising discovery of a new function for A-beta has implications in the search for new treatments for Alzheimer’s disease.

“Proteins don’t have a moral valence. They have functions that are either adaptive or not and it just functions differently in different settings,” Goldstein said. “Now that we understand the settings better and are consequently in a better position to understand how to treat and modulate, the protein may be providing some protective function and important biological functions that we previously didn’t appreciate.”

Moir said that this study has stirred more interest in the role of pathogens in Alzheimer’s disease among other researchers.

“We have discovered a function for this thing that everybody thought was just ‘junk’ and it has opened into whole new potential strategies for treating disease,” he said.

Goldstein also mentioned the debunking of earlier theories about A-beta as one of the significant contributions of his research.

“Overturning dogma is a way of shedding light and moving the field forward,” he said. “Following informed instinct and not following dogma is a cherished thing to keep untarnished.”