Process may help regrow damaged nerve cells

A process triggering the regrowth of damaged nerve cell branches may help improve treatments for injuries that can cause paralysis, U.S. researchers say. Researchers at Washington University School of Medicine in St. Louis have identified a chain reaction involved in the regrowth process in some cells, the university reported Thursday. Nerve cells in the brain and spinal cord are missing a link in this chain reaction -- a protein called HDAC5 -- which may help explain why these cells are unlikely to regrow lost branches on their own, they said. A method of activating HDAC5 in the central nervous system may turn on regeneration of nerve cell branches in this region, where injuries often cause lasting paralysis, they said. "We knew several genes that contribute to the regrowth of these nerve cell branches, which are called axons, but until now we didn't know what activated the expression of these genes and, hence, the repair process," neurobiology Professor Valeria Cavalli said. "This puts us a step closer to one day being able to develop treatments that enhance axon regrowth." Axons, the branches of nerve cells that send messages, are typically are much longer and more vulnerable to injury than dendrites, the branches that receive messages. In the peripheral nervous system -- outside the brain and spinal column -- cells sometimes naturally regenerate damaged axons with the help of HDAC5, but in the central nervous system injured nerve cells typically do not replace lost axons after injury. In central nervous system cells, the protein HDAC5 never reaches the site of the injury; the failure to get this essential player out of the nucleus may be one of the most important reasons why central nervous system cells do not regenerate axons, the researchers said. "This gives us the hope that if we can find ways to manipulate this system in brain and spinal cord neurons, we can help the cells of the central nervous system regrow lost branches," Cavalli said. "We're working on that now."