[Back to Issue 3 ToC] [Back to Journal Contents] [Back to Biochemistry (Moscow) Home page]

Association of Increased Homocysteine Levels with Impaired Folate Metabolism and Vitamin B Deficiency in Early-Onset Multiple Sclerosis


Victoria I. Lioudyno1,a*, Evgenia A. Tsymbalova1, Ekaterina A. Chernyavskaya1, Elena Y. Scripchenko2, Gennadij N. Bisaga3, Alexander V. Dmitriev1, and Irina N. Abdurasulova1

1Institute of Experimental Medicine, 197022 Saint Petersburg, Russia

2Pediatric Research and Clinical Centre for Infectious Diseases, 197022 Saint Petersburg, Russia

3Almazov National Medical Research Center, 197341 Saint Petersburg, Russia

Received October 30, 2023; Revised November 29, 2023; Accepted December 8, 2023
The contents of homocysteine (HCy), cyanocobalamin (vitamin B12), folic acid (vitamin B9), and pyridoxine (vitamin B6) were analyzed and the genotypes of the main gene polymorphisms associated with folate metabolism (C677T and A1298C of the MTHFR gene, A2756G of the MTR gene and A66G of the MTRR gene) were determined in children at the onset of multiple sclerosis (MS) (with disease duration of no more than six months), healthy children under 18 years (control group), healthy adults without neurological pathology, adult patients with MS at the onset of disease, and adult patients with long-term MS. A significant increase in the HCy levels was found in children at the MS onset compared to healthy children of the corresponding age. It was established that the content of HCy in children has a high predictive value. At the same time, an increase in the HCy levels was not accompanied by the deficiency of vitamins B6, B9, and B12 in the blood. The lack of correlation between the laboratory signs of vitamin deficiency and HCy levels may be due to the polymorphic variants of folate cycle genes. An increased HCy level should be considered as a marker of functional disorders of folate metabolism accompanying the development of pathological process in pediatric MS. Our finding can be used to develop new approaches to the prevention of demyelination in children and treatment of pediatric MS.
KEY WORDS: multiple sclerosis, homocysteine, folate metabolism

DOI: 10.1134/S0006297924030143

Publisher’s Note. Pleiades Publishing remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.