-- Robert Preidt
THURSDAY, April 25 (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
"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
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
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
"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."
The U.S. National Institute of Neurological Disorders and Stroke
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