A Duke research study is shedding new light on Alzheimer’s disease.
The study—published April 15 in the Journal of Neuroscience—is attracting national attention for proposing a new potential cause of Alzheimer’s. Duke researchers, who discovered a way to make the brains of mice respond to Alzheimer’s disease similarly to humans, found that in mice with the disease, immune system cells meant to protect the brain start to consume an important nutrient: arginine. They were able to slow the disease’s progress in the mouse model with a small-molecule drug—indicating the eventual potential for a new treatment strategy.
Past research of the disease has focused on a protein called beta-amyloid, which creates “plaques” in the brain, rather than arginine.
“With drugs that affect amyloid, not a single trial has succeeded,” said Carol Colton, an author of the study and professor of neurology at the School of Medicine. “It’s time we look at new direction—and this is a potential direction that nobody has thought of before.”
Although Colton has been researching the immune system’s role in Alzheimer’s for many years, the breakthrough came when she was able to develop a mouse model that was more representative of the disease in humans than other models in the field.
Previously, genetic mutations given to mice led to the development of plaques in the brain, but failed to replicate the most important aspects of Alzheimer’s, including neuron death and memory loss, Colton explained.