Abstract

Background: Advanced glycation end products (AGEs) are involved in the pathogenesis of many diseases, including neurodegenerative diseases such as multiple sclerosis (MS). The aim of the study was to determine serum concentrations of AGEs and their soluble receptor (sRAGE) in MS patients and healthy controls and to investigate their possible influence on disease activity. Methods: Serum concentrations of AGE and sRAGE in patients with MS and healthy controls were determined by enzyme-linked immunosorbent assay (ELISA). Results: The mean serum AGE concentration in patients with MS was higher than in healthy controls, whereas the mean serum sRAGE concentration was lower than in the control group. However, the differences were not statistically significant. In MS patients, serum AGE and sRAGE concentrations did not differ significantly, depending on the duration of the disease and the Expanded Disability Status Scale (EDSS) score. Conclusions: Multiple sclerosis may be accompanied by disturbances of the AGE-sRAGE axis. However, further studies are warranted to confirm it. The duration of the disease and the degree of disability do not seem to affect the progression of the glycation process, particularly in the stable phase of the disease.

Highlights

  • Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease involving the central nervous system [1,2,3,4,5,6,7,8,9], whose etiopathogenesis is not fully understood

  • Important sources of oxidizing species are the reactive oxygen species (ROS)-generating enzymes: myeloperoxidase, xanthine oxidase, and NADPH oxidase [29,31]. Another source of oxidative stress in the central nervous system are enzymes associated with arachidonic-acid signaling; free radicals are produced by cyclooxygenases and lipoxygenase [32,33]

  • Relapsing-remitting multiple sclerosis (MS) was diagnosed in 73% of patients, whereas secondary progressive MS was diagnosed in 27% of subjects

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Summary

Introduction

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease involving the central nervous system [1,2,3,4,5,6,7,8,9], whose etiopathogenesis is not fully understood. The correlations between the increase in the incidence and the increase in latitude in the northern hemisphere as well as decreased incidence in the southern hemisphere were noted [21] It is probably associated with lower serum vitamin D3 concentrations in MS patients [9,22,23,24,25,26,27]. Important sources of oxidizing species are the ROS-generating enzymes: myeloperoxidase, xanthine oxidase, and NADPH oxidase [29,31] Another source of oxidative stress in the central nervous system are enzymes associated with arachidonic-acid signaling; free radicals are produced by cyclooxygenases and lipoxygenase [32,33]. The duration of the disease and the degree of disability do not seem to affect the progression of the glycation process, in the stable phase of the disease

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