Blocking a protein that contributes to nerve damage could potentially slow—or even halt—the progression of multiple sclerosis (MS). Research published in the journal Brain demonstrates the key role played by the collapsin response mediator protein 2 (CRMP-2) in the development of MS. Scientists from Monash University, the University of Toronto, Yale University, and the University of Western Australia discovered that a modified version of CRMP-2 is present in active MS lesions, which indicate damage to the nervous system, in a laboratory model of MS. The modified CRMP-2 interacts with another protein to cause nerve fiber damage that can result in numbness, blindness, difficulties with speech and motor skills, and cognitive impairments in sufferers. When either the modified CRMP-2 or the interaction between the two proteins was blocked, using a method already approved in both the US and Australia, the progression of the disease was halted. “Blocking the same protein in people with MS could provide a ‘handbrake’ to the progression of the disease,” Boyd adds. The method used to block the protein was approved for the treatment of other disease conditions by both the US Food and Drug Administration and Australia’s Therapeutic Goods Administration, notes study co-leader Steven Petratos, who is affiliated with MISCL and RMIT University. “This should mean that clinical trials—once they start—will be fast tracked as the form of administration has already been approved,” Petratos says. The research received major funding from the National Multiple Sclerosis Society of the United States of America and partial funding from MS Research Australia.