The immune system may play a part in Alzheimer's disease, researchers reported Wednesday, in a discovery that could lead to the development of new treatments for the most common form of dementia.

The study, published in the Journal of Neuroscience by authors from Duke University, West Virginia University School of Medicine and the University of Washington found that certain immune system cells, which normally protect the brain, began to consume a key nutrient known as arginine during the early stages of a mouse model of Alzheimer's disease.

In tests on mice, researchers were able use a small-molecule drug, known as difluoromethylornithine (DFMO), to block the arginine consumption process. That, in turn, prevented the development of brain plaques, which can damage and destroy brain cells. As such, it could curtail memory loss, the authors of the report believe.

The study found that while the exact role of immune system cells was unclear, the research could point to a new potential cause of Alzheimer's while eventually opening a door to a new treatment strategy.

"If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease," said Carol Colton, professor of neurology at the Duke University School of Medicine, a senior author of the study. "We see this study opening the doors to thinking about Alzheimer's in a completely different way, to break the stalemate of ideas in Alzheimer's disease."

Research into the brains of Alzheimer's sufferers has typically focused on two types of protein build-up: "plaques" and "tangles." Plaques are a build-up of sticky proteins known as beta amyloid while tangles are a twisted protein called tau.

By studying a type of mouse created several years ago with a similar type of immune system to a human, researchers found that immune cells called microglia began to divide and change early in the onset of Alzheimer's.

In this study, using DFMO on the mice before the onset of Alzheimer's symptoms, scientists were able to block damage caused by arginase, an enzyme that breaks down arginine.

"All of this suggests to us that if you can block this local process of amino acid deprivation, then you can protect — the mouse, at least — from Alzheimer's disease," said Matthew Kan, one of the researchers involved in the study.

While DFMO is being analyzed in clinical trials involving humans for the treatment of some cancers, until now it had not been tested for its potential to treat Alzheimer's. The Duke University researchers are now investigating if DFMO can indeed treat Alzheimer's after it appears.

Dr. James Pickett, head of research at the U.K.-based Alzheimer's Society, said the study offers hope "that these findings could lead to new treatments for dementia."

"This study in animals joins some of the dots in our incomplete understanding of the processes that cause Alzheimer's disease, in particular around the role played by the immune system," Pickett said.

Al Jazeera and Agence France-Presse