Study identifies new drug target for preserving b...( Therefore instead of helping the rel...),Health

To determine whether inflammation would be decreased when IL-1 stimulation is blocked, Levison and his colleagues evaluated brain injury in mice that lacked the capacity to respond to IL-1. In their study of these so-called IL-1 receptor null mice, Levison and his colleagues found that fewer macrophages were attracted to the brain, and that the brain's macrophages, know as microglia, were not as excited and did not produce substances that would harm healthy brain cells.

"These data suggest that cell preservation is achieved by stopping macrophage, or microglial, activation," Levison said. "In addition, the research shows that the initial burst of IL-1 causes more IL-1 to be released, which amplifies the injury response. This causes a runaway inflammation in the brain where you don't want it. It's as David Bowie would put it, 'like putting out the fire with gasoline.' This study helps us understand why inflammation in the brain is not good and specifically why IL-1 is not good for the brain."

Previous studies by a variety of investigators have shown that IL-1 is elevated after traumatic brain injury, multiple sclerosis, Alzheimer's Disease and Downs Syndrome and that mice with reduced IL-1 are significantly protected from ischemic injury brain damage caused by a lack of oxygen reaching the brain. Other research showed that administering a substance that inhibits IL-1 reduced neuronal death after ischemia.

By establishing the cellular and molecular components of the Central Nervous System injury response, Levison's work reveals why inhibiting IL-1 will protect brain cells from injury and disease. Additionally, this research could lead to new drug therapies to preserve brain tissue in people who've suffered a brain injury or stroke, or have a neurodegenerative
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Contact: Valerie Gliem
vgliem@psu.edu
717-531-8606
Penn State
16-Jul-2002