The immune system may play a part in Alzheimer’s disease, US researchers have discovered, in a breakthrough which could lead to the development of new treatments for the most common form of dementia.
A Duke University study published in the Journal of Neuroscience reported on researchers’ findings that certain immune system cells which normally protect the brain began to consume a key nutrient, arginine.
In tests on mice, researchers were able to block the process with a small-molecule drug to prevent brain plaques and memory loss.
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 hallmarks — “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.
Using the drug difluoromethylornithine (DFMO) before the onset of symptoms, scientists were able to block damage caused by arginase, an enzyme which 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.