5th Edition of International Neurology Conference 2026

Abstract

Background: Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system and a leading cause of neurological disability in young adults. Experimental autoimmune encephalomyelitis (EAE) is a widely accepted animal model that reproduces the major pathological features of MS, including neuroinflammation, demyelination, axonal injury, and functional impairment. Increasing evidence suggests that oxidative and nitrosative stress play crucial roles in the progression of demyelinating disorders, with nitric oxide (NO) acting as an important mediator of these pathological processes.

Objective: To investigate the effects of the ganglioside-containing drug Cronassial on nitric oxide metabolism and sulfhydryl group homeostasis in rats with experimental autoimmune encephalomyelitis.

Methods: EAE was induced in rats, and Cronassial, a preparation containing mono-, di-, and tri-sialyl gangliosides, was administered as a therapeutic agent. Nitric oxide levels, reduced sulfhydryl groups, and oxidized sulfhydryl groups were determined to evaluate oxidative and nitrosative stress.

Results: EAE was associated with a significant increase in nitric oxide production, depletion of reduced sulfhydryl groups, and accumulation of oxidized sulfhydryl groups, indicating the development of oxidative and nitrosative stress. These alterations are consistent with mitochondrial dysfunction and may contribute to the progression of neuroinflammatory and demyelinating processes. Treatment with Cronassial partially restored nitric oxide and sulfhydryl group balance, suggesting attenuation of oxidative damage and improvement of cellular redox homeostasis.

Conclusions: Cronassial demonstrated antioxidant and neuroprotective properties in experimental autoimmune encephalomyelitis by modulating nitric oxide metabolism and restoring thiol homeostasis. These findings support the therapeutic potential of ganglioside-containing agents for reducing oxidative damage and slowing the progression of autoimmune demyelinating diseases such as multiple sclerosis.