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Promising Candidates For Therapy In Traumatic Injury To Adult Brain And Spine

  April, 28 2001 4:03
your information resource in human molecular genetics
A clear path to regeneration

Functional recovery after traumatic injury within the adult brain and spine requires that the regenerating nerves cross the site of the injury. Unfortunately, scarring in this area leads to the expression of many proteins that inhibit axon growth.

In this issue of Nature Neuroscience (Vol. 4, No. 5, 01 May 2001), James Fawcett and colleagues show that proteins modified by addition of a class of sugars (known as chondroitin sulfates) are one type of these inhibitory molecules, and that chemical removal of these sugar groups permits regrowth through the injured site.

Their model of traumatic injury is damage to the rat nigrostriatal system, the dopamine-releasing neurons that degenerate in patients with Parkinson's disease. As expected, injury resulted in scarring of the neural tissue, which was accompanied by an increase in the expression of chondroitin sulfate proteins at the injured site. In control animals, essentially no nerve regrowth was seen to cross this scar. However, if the injured area was continuously treated with chondroitinase ABC, an enzyme that removes the inhibitory sugar groups, the dopamine-releasing axons grew across the injured site. Furthermore, these neurons did not grow across the site randomly, but actually grew back to their original target, suggesting that the treatment could, in principal, restore normal function.

Whether true functional recovery is actually obtained will need to be addressed in future studies. However, this work does suggest that enzymes such as chondroitinase ABC are promising candidates for therapy in cases of traumatic injury to the adult brain and spine.


Dr. James W. Fawcett
Physiological Laboratory
University of Cambridge
Downing Site, Tennis Court Road
Cambridge, CB2 3EG
tel: +44 1223 333832
fax : +44 1223 333840
email: jf108@cam.ac.uk

(C) Nature Neuroscience press release.

Message posted by: Trevor M. D'Souza

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