Multiple sclerosis (MS) is a neurodegenerative disease characterized by demyelination of the central nervous system. Young women between the ages of 20 and 40 are primarily targeted by this disabling disorder. Till now there are no sufficient mechanisms to explain the pathophysiology of multiple sclerosis.

Neuroinflammation has been implicated in the initiation and progression of several central nervous system (CNS) disorders, including multiple sclerosis. Microglia and astrocytes are essential in neural development, maintenance of synaptic connections, and homeostasis in a healthy brain. Recent researchers have discovered that microRNAs (miRNAs) contribute to the pathophysiology of MS, primarily influencing glial cells and the immune cells in the periphery. In recent years, miRNAs have become more prevalent as inflammation and demyelination process regulators in MS. miRNAs are naturally occurring, non-coding RNA molecules (21-25 nucleotides). miRNAs play a part in the post-transcriptional regulation of gene expression and silencing of RNA. miRNAs have been discovered to control some physiological processes, as apoptosis, proliferation, differentiation, and development. Measurement of circulating miRNAs in MS patients' peripheral blood is one of the promising approaches as it can be a non-invasive tool to explain its pathogenesis. miRNAs are remarkably stable in bodily fluids and are relatively simple to collect and quantify. Moreover, a novel approach to therapy may be based on methods that regulate the activity of miRNAs. Several miRNAs particularly miR-27 have been reportedly involved in regulating myelination in the central nervous system. However, the role of micro RNAs in generation or progression of MS remains elusive. Follistatin-like protein-1 (FSTL1) was first identified as a transforming growth factor β1-inducible protein. In the last decade, FSTL1 has been identified as a novel inflammatory protein. FSTL1 is a glycoprotein rich in cysteine (SPARC) family. FSTL1 is elevated in various inflammatory conditions and decreased during treatment. Moreover, a variety of studies suggest that targeting of FSTL1 may be useful in the treatment of diseases in which inflammation plays a central role. Recent studies revealed a substantial connection between FSTL1 and micro-RNA 27 levels and demonstrated that the regulatory effects of miR-27 in some inflammatory conditions may be exerted by targeting FSTL1. This study aims to investigate the expression patterns of miR-27 and Follistatin like 1 gene in peripheral blood samples of MS patients. As, we hypothesize that miR-27 and its target gene (FSTL1) may serve important roles in the pathogenesis of MS.