NIH Awards Grant for Molecular TBI Research

Medical News Today

The National Institutes of Health has awarded $1.7 million to a University of Cincinnati (UC) scientist to do molecular research that could lead to better treatments for brain injury patients.

Kenneth Strauss, PhD, will study two types of molecules known as eicosanoids (eye-KO'-sa-noids), which are created by injured brain cells, to confirm that they can actually protect healthy brain cells from further damage.

If successful, Strauss's research could lead to a new class of drugs designed to enhance the levels of these helpful molecules, and thereby improve outcomes in patients who have suffered traumatic brain injury, the leading cause of death and disability among people aged 16 to 45.

"One of my goals," says Strauss, a research associate professor of neurosurgery at UC and director of the Mayfield Neurotrauma Research Lab, "is to develop therapies for traumatic brain injury, a condition for which there is no effective medical treatment."

When the brain suffers traumatic injury, Strauss explains, it automatically takes self-protective action. The brain cells release arachidonic acid, which triggers a series of events that draw additional cells to the injured site.

While some of the compounds resulting from the initial trauma appear to be protective and to inhibit harmful inflammation, Strauss says, others are harmful if they remain for too long. Their fight to save the injured brain can spill over into nearby areas, damaging neighboring structures.

"Brain cells and immune system cells in the blood stream alter their function and essentially gather at the damage site," Strauss says. "They can proliferate and release chemicals that cause the region to swell up. In their effort to either cordon off or repair the damage, they can also constrict blood vessels or attract even more cells into that area."

Thus far doctors have been unable to prevent or manipulate these progressive changes that follow traumatic brain injury.

Strauss and other researchers previously found that the enzyme COX-2 is one of the contributors to harmful inflammation. COX-2 increases following injury and, to the brain's detriment, remains elevated for many days.

Strauss had originally been studying the potential of the arthritis drug Vioxx, a COX-2 inhibitor, for reducing inflammation in the injured brain. But his plan was shelved when Merck withdrew Vioxx in 2004 after clinical trials showed that long-term use increased the risk of heart attack and stroke.

Strauss then shifted his focus from suppression of the harmful COX-2 enzyme to the potential for elevating two theoretically helpful eicosanoids, known as 'HETEs' and 'EETs.'