Story URL: http://news.medill.northwestern.edu/chicago/news.aspx?id=212727
Story Retrieval Date: 9/1/2014 1:34:05 PM CST
Swiss and German researchers were able to turn off particular cytokines, a type of immune system signal transmitters, in older mice using a medicine already approved by the U.S. Food and Drug Administration for psoriasis.
Cytokines surround accumulations of abnormal brain proteins called beta-amyloids. They secrete chemicals that cause inflammation, which past research suggests trigger plaques in Alzheimer’s patients’ brains. The plaques build up and blocks neuron signals, causing the brain’s cortex to shrivel and the hippocampus to shrink.
In this case, scientists showed that minimizing the brain’s immune reaction to beta-amyloids might slow the accumulation of plaques, reducing early Alzheimer’s symptoms and restoring cognitive function, according to researchers.
The researchers encouraged clinical trials using medications that shut down specific immune responses in Alzheimer’s patients. Professor Frank Heppner, with the Charite-Universitatsmedizin Berlin, and his college Burkhard Becher of the Institute of Experimental Immunology at the University of Zurich showed the link between turning off immune system triggers and preventing plaque buildup in the brains of the mice.
Alzheimer’s disease affects an estimated 5.4 million Americans, according to the Alzheimer’s Association, a global health organization and nonprofit research funder. It is the most common type of dementia, a term used to describe memory loss, confusion and other cognitive afflictions that impact quality of living. But Alzheimer's ultimately shuts down other physical functioning as brain function fails and leads to death.
This study might result in future breakthroughs in Alzheimer’s treatment, researchers said. But some physicians caution that that brain inflammation might serve a dual purpose, and that suppressing immune reactions could reduce potential benefits.
The paper provided “additional evidence that inflammation may be important [in Alzheimer’s],” said Dr. Marsel Mesulam, the director of the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University Feinberg School of Medicine.
“Inhibiting this inflammatory reaction in some way or another helps the neural damage in the brain,” Mesulam said.
However, Mesulum added, inflammatory cells might also serve a useful function by “gobbling up” amyloid deposits.
“The inflammatory reaction may, at some level, actually be useful,” Mesulam said.
Dr. Changiz Geula is a research professor at the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University Feinberg School of Medicine, agreed with Mesulam. Geula suggested that future research “enhance [the cytokines] that are protective and inhibit the ones that might cause damage.”
“The inflammation has two sides, there’s no question. One side is good, one is bad,” said Geula. “There are cytokines that are damaging and are associated with plaque formation, but then there are cytokines that are protective as well. So there is definitely a double-edged sword that needs to be acknowleged.”
Geula also warned that studies with transgenic animal subjects do not always show the same results in humans – particularly when it comes to inflammation.
“Rodents can survive all kinds of infections,” Geula said. “We have to wait and see. In the past, a lot of clinical trials have not panned out in the end,” he said. “Personally, I remain pessimistic.”