Apr 11, 2002
NEW YORK (Reuters Health)
Treatment with a monoclonal antibody against a neurite inhibitory protein improves functional recovery in a rat model of ischemic stroke, according to a report published in the April issue of the Annals of Neurology. The mechanism appears to involve enhancement of neuroanatomical plasticity in uninjured brain regions.
In contrast to the developing human brain, the adult brain exhibits limited neuroanatomical plasticity after injury, note Dr. Gwendolyn L. Kartje, from Loyola University Medical Center in Maywood, Illinois, and colleagues. In theory, treatments that increase cortical plasticity could have a beneficial effect on recovery following stroke.
Nogo-A, a neurite inhibitory protein found in adult brains, is one of several molecules that may limit plasticity. In the current study, the investigators treated rats with IN-1, a monoclonal antibody that neutralizes Nogo-A, immediately after middle cerebral artery occlusion. The procedure involved injecting antibody-secreting hybridoma cells posterior to the lesion, with cyclosporin therapy to prevent rejection.
Compared with control animals, IN-1-treated rats demonstrated significantly greater functional recovery on a forelimb-reaching task, the authors note. Furthermore, the brains of treated rats showed new cortico-efferent projections from the opposite, unlesioned hemisphere.
"Strategies that take advantage of the growth potential of the injured central nervous system as well as the permissive environment created by blockade of neurite growth-inhibitory factors may lead to new neuronal pathways and functional recovery in adult patients following ischemic stroke," Dr. Kartje's team concludes.
Ann Neurol 2002;51:433-441.
© 2002 Reuters Ltd