Protein Therapy Could Reverse Damage in Stroke Patients
Nogo-A, a protein that inhibits the growth of nerve fibers, can prevent recovery from stroke damage. Scientists now have a new technique called anti-Nogo-A, which could reverse damage and restore functions lost due to stroke.
Therapy that reverses stroke damage could change lives
Stroke is a leading cause of serious, long-term disability in the United States, and the third largest cause of death, according to the American Heart Association. More than 6.4 million stroke survivors live in the United States, and many of them struggle with the day-to-day challenges associated with a loss of physical functioning.
A new therapy “may be used to restore function even when it’s given long after ischemic brain damage has occurred,” according to Gwendolyn Kartje, MD, PhD, senior author of the new study, and her colleagues. Kartje is director of the Neuroscience Institute of Loyola University Chicago Stritch School of Medicine and chief of neuroscience research at Edward Hines Jr VA Hospital.
An ischemic stroke is the most common type, affecting approximately 80 percent of all stroke patients. Ischemic strokes develop in major blood vessels either on the surface of the brain or in small blood vessels deep in the brain. The other type of stroke is hemorrhagic, which occurs when a blood vessel in the brain ruptures and bleeds into the surrounding tissue.
Anti-Nogo-A therapy disables the Nogo-A protein, a substance that inhibits the growth of nerve fibers called axons. Once anti-Nogo-A puts the brakes on Nogo-A, axons are allowed to grow into the side of the body affected by a stroke and functions formerly “lost” because of the stroke can be restored.
In this new study, Kartje and her colleagues report on the results of an experiment using 15 rats that had medically induced strokes. The rats had been trained to reach and grab food pellets with their front paws. One week after their stroke, the rats had great difficulty grabbing the pellets, and they showed very little improvement over the next two months.
Nine weeks after the stroke, the researchers gave six rats anti-Nogo therapy, four rats received an inactive antibody, and five rats received no treatment. After another nine-week period, the rats that had received anti-Nogo treatment had regained 78 percent of their pre-stroke ability to grab food pellets. Subsequent examination of the rats’ brains showed that the animals had significant sprouting of axons.
Rats that did not receive treatment regained only 47 percent of pre-stroke function, while those that got antibodies regained only 33 percent. The brains of these rats did not show axon sprouting.
Currently, a drug called tPA is a stroke victim’s most promising chance for limiting damage, but it must be administered within the first three hours of the event to reap the most benefit. Discovery of a new protein 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.”
American Heart Association