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Study identifies new drug target for preserving brain cells

Doctors know that the body's natural response to injury inflammation can do more harm than good when it comes to the brain.

But new research from Steven Levison, Ph.D., associate professor of neuroscience and anatomy, Penn State College of Medicine, explains the cellular and molecular reasons why this is true. Furthermore, his research provides important information that could lead to new drugs to prevent brain cell death after injury or as a consequence of neurodegenerative diseases like Alzheimer's.

Levison's study on mice, published in the July 15, 2002, print edition of Journal of Neuroscience, not only describes an important mechanism by which the body reacts to brain injury, but goes farther to show why inhibiting the effects of interleukin-1 a protein immune cells release in response to injury will stop additional brain tissue damage. The article will be released on-line on July 16, 2002.

"The study provides strong rationale for testing IL-1 receptor blocking reagents as treatments for traumatic brain injury and stroke, and even neurodegenerative diseases like multiple sclerosis and Alzheimer's disease," Levison said.

In both mice and humans, IL-1 is a vital component of the injury response. When IL-1 is released into a tissue, it activates scavenger cells known as macrophages to move into the injury site and cause inflammation. Macrophages release substances that kill bacteria and viruses, and they ingest dead cells. They also release IL-1, which signals more macrophages to invade the damaged tissue.

"The macrophage reaction is a good one in regenerating tissues, but in a non-regenerating tissue like the brain, it can be devastating," Levison said.

When macrophages release IL-1 and attract more of the scavenger cells to the brain, they become exited and overactive, causing harm to other cells nearby. This adds to the damage caused by the initial injury and destroys more healthy neurons.
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Contact: Valerie Gliem
vgliem@psu.edu
717-531-8606
Penn State
16-Jul-2002


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