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University of Cincinnati receives $1.7M to research molecular treatment of brain injury

ow 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 brains 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.

We believe eicosanoids reduce the number of inflammatory cells that fester around the injury site and cause chronic tissue degeneration, Strauss says. We think this plays a role in impairment not only after trauma, but also after other brain injuries, including strokes, seizures and the chronic neurodegenerative conditions like Alzheimers disease.

Strauss hypothesizes that manipulating the chemistry of the injured brain cells to favor the creation of the beneficial eicosanoids will aid recovery from traumatic brain injury.

He will first study the phenomenon in rodents that have been genetically manipulated so that they produce either an abundance or an insufficient amount of the molecules.

He will also study unique compounds, provided by colleagues at the University of Texas Southwestern Medical Center and the University of California, Davis, that boost beneficial eicosanoids that occur naturally in the brain. These compounds could set the stage for the development of drugs that would benefit traumatic brain injury patients.


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Contact: Cindy Starr
cstarr@mayfieldclinic.com
513-569-5321
University of Cincinnati
5-Jul-2007


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