The potential for an antidepressant drug to reverse spinal-cord injury has been indicated following lab tests on rats by a scientist from Northern Ireland in New York, writes Jane Qui
Researchers have found that a drug first developed as an antidepressant could aid recovery from spinal-cord injury. In a study published in the US Proceedings of National Academy of Science, the researchers injected rolipram under the skin of injured rats for 10 days following spinal cord trauma. One month later, animals treated with the drug had much improved use of their limbs and paws.
The work was carried out by Dr Marie Filbin at Hunter College, City University of New York. Filbin was born and brought up in Lurgan, Co Armagh, and is the only female winner of the prestigious Ameritec Award for Spinal Cord Research.
"We are very excited by the extent of recovery the animals achieved," says Dr Filbin. "This is rather encouraging. But it is only a small step towards solving a very complicated problem."
Many tissues of the body - skin, bone and gut - can repair and restore function after injury. The brain and spinal cord are the exceptions. The search for the reason behind this led to the discovery.
"There are many reasons why adult spinal cord does not regenerate. We have focused on a molecule in the nerve cell called cAMP," Filbin explains. "cAMP is like the molecular fuel that steers the growth of nerve fibres. Nerve cells from newborn animals have plenty but, as the cells grow older, the amount drops sharply."
The research team already knew that new-born animals, rats at least, could recover from spinal cord injury without much difficulty.
"So we conjectured that adult nerve cells might be in shortage of the 'fuel'. If this is correct then giving adult cells a 'refuel' may encourage them to grow better after injury," she says.
Instead of adding more cAMP to the cells, the researchers took advantage of the drug rolipram that prevents the breakdown of cAMP in the cell and, in effect, increases its levels. They also transplanted embryonic tissues at the injury site to provide an amicable environment for growth.
"We found that the rolipram treatment resulted in more growing nerve fibres in the damaged spinal cord. On the contrary, severed nerve fibres in untreated animals retracted from the injury site and eventually died out," says Filbin.
"The advantage of rolipram is that it can cross the blood-brain barrier, which is ideal for treating brain conditions," she explains.
Although rolipram is already approved by the US Federal Drug Administration for treating depression and memory disorders, it causes severe vomiting.
Therefore, if this approach proves promising, the bad side-effects must be addressed before clinical trials can start for spinal cord injury.
Rolipram can also counter inflammation, and clinical trials are under way in both the US and Europe to treat some forms of Multiple Sclerosis.
"There was less scar tissue in the damaged spinal cord of rolipram-treated animals," says Filbin. "This may be an indication that inflammation was also dampened in those animals."
Scientists believe that the dense scar tissues formed after spinal cord injury could be a physical barrier to any regenerative attempts of damaged nerve fibres.
"Rolipram may be a stone that can kill two birds," Filbin adds.
"We still need to see whether our findings also apply to humans. Even if they do, rolipram is not going to be the magic bullet that can make Superman get up and walk tomorrow," cautions Filbin.
"No single treatment will be effective enough. A combination of various therapies will be necessary to bring about big improvements."