| Breakthroughs in genetic studies, like whole
human genome sequencing and genome-wide association
studies (GWAS), have richened our knowledge of
etiopathology of autoimmune diseases (AID) through discovery
of genetic patterns. Nonetheless, the precise etiology
of autoimmune diseases remains largely unknown. The
lack of complete concordance of autoimmune disease in
identical twins suggests that non-genetic factors also play a
major role in determining disease susceptibility. Although
there is no certain definition, epigenetics has been known
as heritable alterations in gene function without changes in
the nucleotide sequence. DNA methylation, histone modifications,
and microRNA-associated gene expression suppression
are the central mechanisms for epigenetic
regulations. Multiple sclerosis (MS) is a disorder of the
central nervous system (CNS), characterized by both
inflammatory and neurodegenerative features. Although
studies on epigenetic alterations in MS only began in the
past decade, a mounting number of surveys suggest that
epigenetic changes may be involved in the initiation and
development of MS, probably through bridging the effects
of environmental risk factors to genetics. Arming with
clear understanding of epigenetic dysregulations underpins
development of epigenetic therapies. Identifying agents
inhibiting the enzymes controlling epigenetic modifications,
particularly DNA methyltransferases and histone
deacetylases, will be promising therapeutic tool toward
MS. In the article underway, it is aimed to go through the
recent progresses, attempting to disclose how epigenetics
associates with the pathogenesis of MS and how can be
used as therapeutic approach. |