Cancer drug shows promise in regeneration of spinal cord injuriesPublished On: Sat, Jan 29th, 2011 | Photo Gallery / Stem Cell Research | By BioNews
Scientists have shown that cancer drug Taxol reduces regeneration obstacles after a spinal cord injury.
After a spinal cord injury a number of factors impede the regeneration of nerve cells. Two of the most important of these factors are the destabilization of the cytoskeleton and the development of scar tissue. While the former prevents regrowth of cells, the latter creates a barrier for severed nerve cells.Taxol, the trade name of a drug currently used for cancer treatment, has now been shown to promote regeneration of injured central nervous system (CNS)-nerve cells.
The Taxol promotes regeneration of injured CNS-nerve cells in two ways: Taxol stabilizes the microtubules so that their order is maintained and the injured nerve cells regain their ability to grow.
In addition, Taxol prevents the production of an inhibitory substance in the scar tissue. The scar tissue, though reduced by Taxol, will still develop at the site of injury and can thus carry out its protective function. Yet growing nerve cells are now better able to cross this barrier.
Experiments in rats performed by this group verified the effects of Taxol. These researchers supplied the injury site after a partial spinal cord lesion with Taxol via a miniature pump. After just a few weeks, animals showed a significant improvement in their movements.
“So far we tested the effects of Taxol immediately after a lesion”, explains Farida Hellal, the first author of the study.
The study has been published in the online issue of the journal Science. (ANI)
Microtubule Stabilization Reduces Scarring and Causes Axon Regeneration After Spinal Cord Injury
Farida Hellal, Andres Hurtado, Jörg Ruschel, Kevin C. Flynn, Claudia J. Laskowski, Martina Umlauf, Lukas C. Kapitein, Dinara Strikis, Vance Lemmon, John Bixby, Casper C. Hoogenraad, and Frank Bradke
Science 1201148Published online 27 January 2011 [DOI:10.1126/science.1201148]