Martin Samohýl, Ľubomír Lisý, Roman Rams, Katarína Hirošová, Diana Vondrová, Daniela Krajčová, Alexandra Filová, Jana Jurkovičová
Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), characterized by demyelination
and axonal degeneration. Epigenetics is defined as genetic change, which does not occur due to changes
in the DNA sequence. Epigenetics, or changes in genes expression may have a greater impact on the development and
progression of SM than a mutation at a particular locus. Nutritional deficits in childhood may constitute a transgenerational
responses and transgenerational genetic defects. It is believed that MS may have epigenetic origin. Epigenetic
modified genes as the consequences of nutritional factors are related to neurodegeneration. Studies of human neuroblastoma
cells showed epigenetic changes resulting in increased production of beta peptide as a consequence of reduced
vitamin B intake. Coenzyme Q10 has the positive effect on the MS treatment, patients had significantly reduced the
malondialdehyde (MDA) levels. Vitamin A 25,000 IU/day reduces the myelin oligodendrocyte glycoprotein (MOG) levels
induced by T cells proliferation. MS patients, who take calcium in dosage 1,200 mg/day and vitamin D3 in the range
from 28,000 to 280,000 IU/once a week, had reduced T cells reactivity and relapses reduction. Multiple sclerosis is often
associated with vitamin B12 deficiency. It demonstrates the significant relationship with heredity algorithm. Haplotypes
containing the major histocompatibility complex DR beta 1 (HLA-DRB1)*15 have predictive value for genetic
risk. Epigenetic changes are likely to be involved in the process of oligodendrocytes damage in the MS pathogenesis.