Researchers at Yale Medical School are continuing to make strides in the field of neurological research with their discovery of a potential treatment for spinal cord injury and other debilitating illnesses.
The team of scientists, led by neurologist Dr. Stephen Strittmatter, are studying the causes of neural plasticity, the characteristic that allows cells to take on shape and form. Their findings will be printed in an upcoming issue of the publication Science.
Strittmatter’s team attacked this challenge from the perspective of injuries such as spinal cord trauma and strokes, which destroy neurons. During brain development, he said, countless connections are made between neuron-heavy gray matter and white matter, where myelin, the fatty substance that covers certain axons, is found. Yet in adults, the brain loses plasticity, and cannot make these connections, which means it will not be able to reconstruct these ties between white and gray matter in the case of an injury.
For the past several years, the Strittmatter lab has been studying the properties of myelination, or the process of covering the axons with myelin. Their current research describes a novel property in myelin, the presence of inhibitory proteins that end plasticity, or in this case, prevent injury correction.
“So if these inhibitors prevent you from recovering from an injury, why on earth would they exist?” Strittmatter said. “What is their natural function?”
Strittmatter said the inhibitors may lock the neural connections into place until puberty. His research using the visual system of rodent models demonstrated that one protein inhibitor, NOGO, is involved in plasticity loss.
“If you patch one eye during the development phase, the cortex will rearrange,” Strittmatter said.
The eye experiment shows the brain’s plasticity before puberty. But the mice without NOGO had longer periods of plasticity, which allowed the brain to repair itself in adulthood, well beyond puberty. Strittmater’s work provides the prospect for treatment against spinal cord injury, strokes and possibly other brain injuries after development. The idea of causing neurons to grow back in the adult brain does not exist in any current treatments, but Strittmatter said the possibility of initiating human trials for this type of treatment is not very far off.
“[This research] examines the critical period physiologically from eye-opening to puberty,” Nigel Daw, co-author and professor of ophthalmology at the School of Medicine, said.
The research suggests the reason behind a loss of plasticity is that negative factors like the NOGO are already inhibiting and closing down during that critical period.
“If possible, we would like to actually see the anatomical changes from a loss of plasticity and to work out the relationships between these negative factors,” Daw said.
A National Spinal Cord Injury Association spokesman said he welcomes this kind of treatment, especially if it becomes available at trauma centers. Most treatment options for spinal cord injury are invasive and must be administered soon after injury occurs. But the spokesman said any potential improvement will have a dramatic impact on regaining function.