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|Articles|May 1, 2004

UF researchers restore spatial deficits in rats

Gainesville, Fla.-Building on years of basic science that helped pinpoint a region of the rat brain that affects spatial awareness, University of Florida (UF) researchers are now testing the ability of antibodies to restore brain function after a simulated stroke.

Gainesville, Fla.-Building on years of basic science that helped pinpoint a region of the rat brain that affects spatial awareness, University of Florida (UF) researchers are now testing the ability of antibodies to restore brain function after a simulated stroke.

Scientists studying rats with spatial neglect syndrome, a cognitive disorder associated primarily with stroke in people, found that injections of monoclonal antibodies into damaged regions of the animals' brains encouraged existing neurons to sprout new growth and restored normal spatial perception as assessed by observing behavior over a period of weeks.

The National Institute of Mental Health recently awarded Roger Reep, Ph.D and James Corwin, Ph.D of Northern Illinois University, a three-year grant renewal totaling $989,000 for their ongoing research.

"What we've found is that the regions of the brain in which neglect syndrome occurs in humans have corresponding regions with similar function in rats," says Reep, a professor of physiological sciences with UF's College of Veterinary Medicine and a member of UF's McKnight Brain Institute. "This means we can investigate mechanisms of neural repair, and so there's hope for developing a therapy to promote recovery in humans. That's the key insight."

UF scientists use monoclonal antibodies, which interfere with the tendency of a naturally occurring protein to block neuron growth, in the laboratory. Researchers elsewhere already had shown the approach could restore movement in rats with spinal cord injuries. Never before, however, has the antibody, known as IN-1, been studied in relation to spatial neglect syndrome.

"In binding to the protein, the antibody keeps the protein's growth-inhibiting characteristics from working as they would naturally in that particular region of the brain following brain injury," says Joe Cheatwood, a graduate student in Reep's laboratory.

"Our work is not directly clinical, but is designed to be, hopefully, translational, in that someone designing clinical trials in people would be able to know that to expect for cognitive problems, such as those seen in our neglect model," he adds.

"The next step for this work is to combine a stroke model with the use of antibodies and stem cells, in an attempt to create the most favorable conditions for restoration of lost neural connections and behavioral recovery of function," says Reep.


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