Published on: April 25, 2013
by HealthDay News:
Insight into genes that play a key role in disrupting immune system pathways in the brains of people with Alzheimer’s disease could offer a potential target for new drugs against the disease, two new studies show.
“Defining the precise steps of the inflammatory response crucial to causing Alzheimer’s disease has been elusive. We are pleased to discover these novel insights into that process,” Bin Zhang, lead author of one of the studies and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mount Sinai in New York City, said in a school news release.
In the study, Zhang’s team analyzed brain tissue samples from deceased Alzheimer’s patients, as well as healthy people who had died. By measuring the activity level of thousands of genes in these tissue samples, the team identified which gene networks are disrupted in diseased brains.
Specifically, their analysis pinpointed the important role of a gene expressed in immune cells called microglia, which clean up debris and destroy pathogens in the brain.
This gene, called TYROBP, is overactive in the brains of Alzheimer’s patients and plays a major role in disrupting the activity of many other genes that control microglia activation, according to the study, which was published April 25 in the journal Cell.
“As a next step, we will evaluate drugs that impact [this] pathway as potential therapies for the disease,” Zhang said. “This discovery enables us to design more specific compounds that target these key steps precisely, in contrast to existing anti-inflammatory drugs that may be less ideal for hitting this target.”
Another study, published online April 25 in the journal Neuron, may have uncovered another genetic clue to Alzheimer’s disease.
Researchers looked at brain samples from deceased Alzheimer’s patients and found that higher activity of a gene called CD33 in microglia was linked to higher levels of the beta-amyloid protein plaques that have long been associated with Alzheimer’s disease.
In their experiments with mice, switching off CD33 activity seemed to help microglia sweep away the plaques.
“Our findings suggest that pharmaceutical inactivation of CD33 represents a potentially powerful new therapy for the treatment and prevention of Alzheimer’s disease, and perhaps other neurodegenerative disorders,” senior study author Rudolph Tanzi, of Massachusetts General Hospital and Harvard Medical School in Boston, said in a journal news release.
Another expert said the findings from both studies may help advance research.
“We have known for a long time that Alzheimer’s disease is characterized by the presence of excessive inflammation in the brain,” said Philippe Marambaud, an investigator at the Litwin-Zucker Research Center for the Study of Alzheimer’s Disease at the Feinstein Institute for Medical Research in Manhasset, N.Y.
“The role of this inflammatory response in the pathogenic mechanisms of the disease, however, remains unclear,” he said. “These two studies … provide concordant evidence that the immune cells microglia actively participate in this disease process.”
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