The groundbreaking preclinical study was written by researchers from Case Western Reserve University and UC, and it was published in the journal Cell Reports.
An innovative new study from the University of Cincinnati offers hope that a new medication could aid in the repair of stroke-related damage. There are currently no FDA-approved medications that can reverse the effects of a stroke.
In an animal model of severe ischemic stroke, the study discovered that the medication NVG-291-R facilitates nervous system repair and considerable functional recovery. Similar effects on brain stem cells are seen when the drug’s molecular target is genetically deleted.
“We are very excited about the data showing significant improvement in motor function, sensory function, spatial learning, and memory,” said Agnes (Yu) Luo, Ph.D., associate professor in the Department of Molecular Genetics and Biochemistry in UC’s College of Medicine and the study’s senior author. Most therapies being researched today primarily focus on reducing the early damage from stroke,” Luo said. “However, our group has focused on neuro repair as an alternative and now has shown that treatment with NVG-291-R not only results in neuroprotection to reduce neuronal death but also robust neuro-reparative effects.”
If the preliminary findings are replicated in clinical settings, the medicine would represent a “major breakthrough,” according to Luo.
The research also revealed that the medication worked even when administered up to seven days after the stroke’s beginning.
To ascertain whether the medication is as effective in repairing the harm caused by ischemic strokes in human patients, additional research and validation of findings from independent groups will be required.
According to Luo, the sole medicine that the FDA has been approved for the treatment of stroke does not repair damage and must be given within 4.5 hours of the stroke’s commencement.
The majority of treatments under investigation must be used within 24 to 48 hours of a stroke’s beginning. The paradigm for stroke treatment would alter if there were a substance that could restore stroke damage even a week after the onset of symptoms.
Professor of neurosciences at CWRU’s School of Medicine and study co-author Jerry Silver, Ph.D., said the research demonstrated that the drug repaired damage through at least two mechanisms: by fostering the migration of newly formed neurons arising from neuronal stem cells to the area of the impairment and by forming new neuro pathways.
“NVG-291-R’s ability to enhance plasticity was demonstrated by using staining techniques that clearly showed an increase in axonal sprouting to the damaged part of the brain,” Silver said. “This enhanced plasticity is an excellent validation of the same powerful mechanisms that we and other researchers were able to demonstrate using NVG-291-R in spinal cord injury.”
Further research is required to determine whether NVG-291-R is capable of efficiently repairing harm brought on by hemorrhagic strokes for all animal models and human patients.
NVG-291 is being tested in a Phase 1 clinical trial on healthy human volunteers.
Parvathy Sukumaran 
