Public Release: 

FGF-2 to the rescue following traumatic brain injury

JCI Journals

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 loss of existing neurons while simultaneously increasing the proliferation of new neurons in this region of the brain.

The data suggest that FGF-2 supplementation might provide a rational strategy to treat brain injury by simultaneously enhancing neurogenesis and reducing neurodegeneration.

In an accompanying Spotlight article on neurogenesis and brain injury, Daniel A. Peterson and colleagues from Chicago Medical School discuss the most recent developments in managing renewable cells for post-injury brain repair.

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TITLE: FGF-2 regulates neurogenesis and degeneration in the dentate gyrus after traumatic brain injury in mice

AUTHOR CONTACT:
Michael A. Moskowitz
Massachusetts General Hospital, Charlestown, Massachusetts, USA.
Phone: (617) 726-8442
Fax: (617) 726-2547
E-mail: Moskowitz@helix.mgh.harvard.edu

View the PDF of this article at: http://www.jci.org/cgi/content/full/112/8/1202

ACCOMPANYING SPOTLIGHT:
Neurogenesis and brain injury: managing a renewable resource for repair

AUTHOR CONTACT:
Daniel A. Peterson
Department of Neuroscience, The Chicago Medical School, North Chicago, Illinois, USA.
Phone: (847) 578-3411
Fax: (847) 578-8545
E-mail: daniel.peterson@finchcms.edu

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