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 prolife
Contact: Brooke Grindlinger
Journal of Clinical Investigation