# Therapeutics Potential of Cronassial in Experimental Autoimmune Encephalomyelitis: Insights Into Glycosphingolipids and Humoral Immunity

**Authors:** Gayane Ghazaryan, Hasmik Zanginyan, Maria Ghazaryan, Laura Hovsepyan

PMC · DOI: 10.1155/tswj/9108462 · 2025-07-18

## TL;DR

This study explores how Cronassial, a drug containing gangliosides, may help treat multiple sclerosis by reducing inflammation and protecting nerve cells.

## Contribution

The study reveals Cronassial's neuroprotective effects by regulating glycosphingolipid metabolism and humoral immunity in EAE.

## Key findings

- Elevated proinflammatory cytokines contribute to EAE pathogenesis and trigger apoptosis.
- Cronassial normalizes cytokine levels and reduces APO-1/Fas concentration, showing neuroprotection.
- The drug modulates glycosphingolipid metabolism and humoral immune factors in EAE.

## Abstract

Currently, significant attention is being paid to the study of the mechanisms underlying the development of multiple sclerosis (MS), especially factors related to humoral immunity, apoptosis, and sphingolipid metabolism processes. These factors play a key role in neuroinflammation and neurodegeneration during both the acute and chronic stages of the disease. The aim of this study was to investigate the concentration of proinflammatory cytokines (IL-1β, IL-6, and TNFα) in plasma, homogenates of the brain and spinal cord, serum circulating immune complexes (CICs), the apoptosis marker APO-1/Fas, and the content of glycosphingolipids during experimental autoimmune encephalomyelitis (EAE) and its treatment. The therapeutic agent used in this study was Cronassial, which contains mono-, di-, and trisialylated gangliosides. Our results indicate the significant role of elevated proinflammatory cytokine levels in the pathogenesis of EAE, which initiate the activation of the sphingomyelin cycle and subsequently trigger apoptosis processes. During the study, we observed an increased concentration of APO-1/Fas. Administration of the ganglioside-containing drug in vivo led to the normalization of the levels of the studied factors, demonstrating a neuroprotective effect. According to our findings, this drug regulates the metabolism of glycosphingolipids and the humoral immune factors that were studied.

## Linked entities

- **Chemicals:** IL-6 (PubChem CID 165368475)
- **Diseases:** multiple sclerosis (MONDO:0005301), experimental autoimmune encephalomyelitis (MONDO:0005134)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, FAS (Fas cell surface death receptor) [NCBI Gene 355] {aka ALPS1A, APO-1, APT1, CD95, FAS1, FASTM}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** MS (MESH:D009103), neuroinflammation (MESH:D000090862), neurodegeneration (MESH:D019636), EAE (MESH:D004681)
- **Chemicals:** Glycosphingolipids (MESH:D006028), ganglioside (MESH:D005732), sphingomyelin (MESH:D013109), mono-, di-, and trisialylated gangliosides (-), sphingolipid (MESH:D013107), Cronassial (MESH:C037470)

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12297129/full.md

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Source: https://tomesphere.com/paper/PMC12297129