Abstract

We examined the sera of 56 patients with definite multiple sclerosis (MS) and 44 healthy individuals using ELISA, for investigating the probable correlation between IgM antibodies against GM1, GD1b and GQ1b gangliosides and clinical parameters of MS. Patients revealed pathological concentrations of the examined antibodies, while healthy controls demonstrated normal levels (p=0.0005). A probable correlation between anti-GD1b and anti-GM1 IgM levels with the progression of MS and a positive comparison between the duration and the disability have also been indicated. Further investigation should be established in order to provide insights on the potential autoantigenic role of gangliosides in MS.

Highlights

  • Gangliosides are acidic glycosphinolipids which are mainly present in neural membranes

  • We examined the anti-GM1 IgM, anti-GD1b IgM and anti-GQ1b IgM serum levels of 56 multiple sclerosis (MS) patients setting the cut of value >25 Eu/ml (Table 1a, Figure 2a-c)

  • In the healthy control group 82% revealed normal anti-GM1 IgM in the serum providing a statistically significant difference (U=121.0, Z=-7.718, p=0.0005)

Read more

Summary

Introduction

Gangliosides are acidic glycosphinolipids which are mainly present in neural membranes (especially in presynaptic membranes). In addition to their role as surface markers in the outer leaflet of cell membranes, gangliosides are thought to have multiple biological functions. A specialized role for gangliosides is the binding of amyloid β protein, a pathological hallmark in Alzheimer’s disease [1,2]. Gangliosides are known to be receptors for myelin-associated glycoprotein (MAG), an enhancer of axon-myelin stability, and a potent inhibitor of axonal degeneration (after injury) [10,11,12]. GT1b, GD1a and GQ1bα appear to be potent support molecules for MAG, while GD3 does not bind [10,13]

Methods
Results
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.