In the October 15 issue of the Journal of Clinical Investigation, Michael Moskowitz and colleagues from Harvard Medical School report that fibroblast growth factor-2 (FGF-2) plays a critical role in the ability of the brain to make new cells following traumatic brain injury (TBI). The authors also demonstrate that administration of FGF-2 boosts the production of new brain cells and protects existing neurons from degeneration following injury. The study suggests that FGF-2 supplementation may improve the outcome of individuals who suffer TBI following motor vehicle accidents or other brain injuries.

The brain can be distinguished from other organs and tissues of the body by its limited ability to repair itself. This lack of self-repair following TBI or disease can often result in severe deficits in cognitive, physical, and psychological skills.

However, in the last several decades, mounting evidence has led to the view of the brain as a dynamic, plastic organ, endowed with some potential for self-repair and regeneration. Recent progress in understanding continued neurogenesis the generation of new neurons (nerve cells) - in the adult brain has raised hopes that self-renewal leading to structural repair by new neurons may even be possible.

Moskowitz and fellow researchers examined the role of FGF-2 in the regulation of neurogenesis and neuron loss in a specific region of the brain known as the hippocampal dentate gyrus (DG), in an animal model of TBI. Mice lacking FGF-2, showed a decreased ability to protect existing neurons and generate new neurons following TBI, when compared to controls, indicating that FGF-2 plays a critical role in stabilizing cell loss following injury.

In an effort to limit cell loss and enhance cell proliferation in the DG following TBI, the authors administered FGF-2 by gene delivery and found that this method was indeed able to limit the
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Oct-2003