Alzheimer’s disease may be linked to misfiring immune system, study reveals
Researchers have found that some immune cells designed to protect the brain from infection start consuming an amino acid called arginine, triggering the onset of classical hallmarks of the disease, including brain plaques and memory loss.
The study, carried out by researchers at Duke University and
published April 15 in the Journal of Neuroscience,
demonstrated that particular immune cells that are meant to
protect the brain start to become destructive and consume an
essential nutrient known as arginine.
Senior author Carol Colton, professor of neurology at the Duke University School of Medicine, said the new research not only indicates the potential cause of Alzheimer’s, but also may eventually lead to a new treatment therapy.
“If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease,” Colton said in the Duke University press release.
"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."
People who suffer from Alzheimer’s show ‘plaques’ and ‘tangles’ inside of the brain that researchers have long mystified researchers. The plaques are an accumulation of sticky proteins called beta amyloid, and tangles are “twisted strands of a protein called tau.”
However, laboratory tests on mice have demonstrated that the drug, difluoromethylornithine, (DFMO) stops the onset of full-blown Alzheimer’s, as well as improving the memory of animals who already had the disease.
Scientists involved in the research expressed surprise by the results.
"It's surprising, because suppression of the immune system is
not what the field has been thinking is happening in Alzheimer’s
Disease," said Matthew Kan, the study’s first author and
MD/PhD student under Colton’s direction.
“Instead, scientists have previously assumed that the brain releases molecules involved in ramping up the immune system, that supposedly damage the brain," he said.
"All of this suggests to us that if you can block this process, then you can protect, the mouse, at least, from Alzheimer's disease.”