Jump-starting nerve fiber growth can lead to huge advancements in regaining of post-stroke mobility.
As a general rule, we at HCPLive.com tend to stay away from covering the results of animal studies, as most either never make to human studies—let alone products or techniques that see the light of day—or fail miserably once they do because of unforeseen side-effects, etc. But, every now and then, a study comes along with such encouraging results, that we just can’t help reporting on them. A study looking at a new technique for jump-starting nerve fiber growth is one of them.
With results that will be published in the January 7, 2011 issue of Stroke, the study found that such a jump-start can reverse much of the damage caused by strokes.
"This therapy may be used to restore function even when it's given long after ischemic brain damage has occurred," senior author Gwendolyn Kartje, MD, PhD, director, Neuroscience Institute, Loyola University Chicago Stritch School of Medicine, and chief, neuroscience research, Edward Hines Jr. VA Hospital, and colleagues wrote.
With doctors left with little to be done to limit stroke damage after the first 24 hours following the stroke, and tPA only limiting damage if administered during the first three hours (most patients don’t receive treatment that quickly), Kartje’s team looked into a treatment called anti-Nogo-A therapy. The therapy fights the protein Nogo-A, which inhibits the growth of axon nerve fibers and “serves as check on runaway nerve growth that could cause a patient to be overly sensitive to pain, or to experience involuntary movements (The protein is called Nogo because it in effect says "No go" to axons.) In anti-Nogo therapy, an antibody disables the Nogo protein. This allows the growth of axons in the stroke-affected side of the body and the restoration of functions lost due to stroke.”
For their study, the researchers medically induced strokes in lab rats and trained them to reach and grab food pellets with their front paws. All animals displayed significant deficits in grabbing pelts with their stroke-impaired limbs at one week post-stroke, with little improvement seen over the following eight weeks.
At nine weeks post-stroke, six rats received anti-Nogo therapy, four received a control treatment that consisted an inactive antibody, and five received not treatment. Nine weeks later (at 18 weeks post-stroke), those rats in the anti-Nogo group regained 78% of their ability to grab pellets, rats in the no treatment group regained 47%, and rats in the control group regained 33%. After examining the brain tissues of rats in the anti-Nogo group, the researchers found significant sprouting of axons.
Anti-Nogo therapy "can induce remarkable compensatory sprouting and fiber growth, indicating the responsiveness of the chronically injured brain to form new neural networks under the proper growth conditions," wrote Kartje and colleagues, adding that their findings “are of great clinical importance," and that the therapy “may benefit not only victims of spinal-cord injury or patients in the early stage of stroke recovery, but also patients in later stages who suffer from neurological disability due to brain damage from stroke or other causes."
Are these results encouraging to you and your patients? Does Anti-Nogo therapy have the potential to see the light of day? Can you imagine a day when stroke patients can regain nearly 80% of their mobility and strength more than four months after suffering a stroke? We’ll keep an eye on Anti-Nogo’s progress and keep you informed. We’re excited about this one!