Vision Loss Prevention in Patients with Multiple Sclerosis
A new therapeutic agent prevented neuronal damage and preserved function in an MS mouse model.
Scientists may have found a way to prevent vision loss in patients with multiple sclerosis (MS).
Optic neuritis is the demyelinating inflammation of the optic nerve, which causes mild to moderate permanent loss of vision, but rarely complete blindness. Approximately half of patients living with MS experience optic neuritis, and for some, it can even be the first symptom of their chronic disease.
In a study published in Scientific Reports, the investigators used a mouse model of MS to demonstrate the therapeutic potential of the agent ST266—–a solution of molecules that stimulates paracrine signaling.
“In this case, the idea is that the many factors in ST266 not only bind to cell receptors and cause changes within the cells they bind to, but those cells then alter their own secretions and provide additional signals to other neighboring cells, thus propagating an effect from a relatively small amount of protein present in the therapy itself,” said lead investigator Kenneth Shindler, MD, PhD. “To the best of our knowledge, this study demonstrates, for the first time, the ability to treat the optic nerve via the intranasal route of administration.”
The investigators administered a nasal dosage of ST266 to the mice with MS. Within 30 minutes, the agent reached the central nervous system, and was detected at higher concentrations in parts of the eye and optic nerve compared with other areas of the brain.
The findings indicate that this type of delivery method could target tissues of the eye, an approach that is easier, less painful, and less invasive then injecting medication directly into the eye.
In the mouse models with optic neuritis, early treatment with ST266 was found to prevent damage and dysfunction, marked by a significant reduction in the loss of optic nerve cells, and suppression of inflammatory cell infiltration into the optic nerve. Thereby, it was associated with limitation of the degree of demyelination caused by MS-related optic neuritis.
“[However], it’s not known if these effects are independent effects of the therapy or interdepended effects,” Shindler said.
The investigators also performed the treatment on mice with later-stage optic neuritis. The treatment demonstrated similar results, which lead to in improved visual function compared with untreated groups. According to the authors, the findings suggest that ST266 helps promote optic neuron survival by potentially activating multiple pathways, including those that prevent apoptosis.
“These results are particularly important as the preservation of retinal cells is a significant factor when treating optic neuritis,” Shindler said. “There is an increased need for combination treatment options that are able to prevent nerve-cell axon loss for patients with optic neuritis.”
Currently, the only acute treatment for MS-related optic neuritis is IV steroids. According to the investigators, this form of treatment only hastens the amount of visual recovery that will occur even without treatment. Furthermore, steroids are unable to prevent nerve damage or permanent vision loss.
“ST266’s ability to preserve vision in the preclinical model and reduce neuronal loss would be a huge advance if it translates to human patients,” Shindler said.
The authors noted that the study findings may show promise in diseases other than MS-related vision issues.
“We also showed an effect on cultured neurons, suggesting that effects may translate to other optic nerve diseases, as well as other brain neurodegenerative diseases,” Shindler concluded.