Epigenetics: Implication on Multiple Sclerosis

The pathogenesis of Multiple sclerosis is not singly identified or entirely understood; however, it is hypothesized to be a multifactorial acquired disease influenced by environmental, genetic, and epigenetic modifications. Epigenetics results in altered gene expression without altering the genetic code and does so by three primary mechanisms: DNA methylation, histone code modifications, and miRNA-regulated gene expression. DNA methylation adds methyl groups to cytosine residues, primarily at CpG dinucleotides, altering chromatin structure to silence genes or repress transcription. Meanwhile, histone code modifications, including acetylation, methylation, phosphorylation, and ubiquitination of histone tails, can limit chromatin accessibility and gene expression. Additionally, miRNAs, small non-coding RNAs, post-transcriptionally regulate gene expression by binding to target mRNAs, either inhibiting translation or promoting mRNA degradation. Dysregulation of these epigenetic mechanisms is implicated in various diseases, such as multiple sclerosis (MS), emphasizing the importance of understanding their intricate interplay in disease development and progression.