Increase in NF-κB-sensitive miRNA-146a and miRNA-155 in multiple sclerosis (MS) and pro-inflammatory neurodegeneration.

Walter J. Lukiw,Jesus F. Lovera,Deidre J. Devier

doi:10.3389/fnmol.2015.00005

Abstract

OPINION article Front. Mol. Neurosci., 02 March 2015Sec. Brain Disease Mechanisms Volume 8 - 2015 | https://doi.org/10.3389/fnmol.2015.00005

Highlights

OVERVIEW Multiple sclerosis (MS) is a complex, debilitating, immunopathologic disease of the human central nervous system (CNS) characterized by chronic systemic inflammation, alterations in innate-immune signaling, progressive demyelination and axonal loss
MULTIPLE SCLEROSIS—INCIDENCE, SYMPTOMS, AND AUTOIMMUNITY To understand the contribution of miRNA-146a and miRNA-155 to the etiopathogenesis of MS we will briefly highlight some salient features of this autoimmune disease
Consistent observations at the pathogenic and molecular-genetic level indicate five main highly interactive characteristics of MS: (i) a progressive demyelination whose extent correlates to MS severity; (ii) axonal swelling and macrophage activation; (iii) a T-cell mediated inflammatory response that subsequently triggers immune cells to release pro-inflammatory cytokines such as IL-1β; (iv) permeability changes in the blood–brain barrier (Kamphuis et al, 2015); and (v) increases in proinflammatory microRNA and related pathogenic biomarkers (Haghikia et al, 2012; Meinl and Meister, 2012; Danborg et al, 2014; Harris and Sadiq, 2014; Küçükali et al, 2014; Ma et al, 2014; Sturm et al, 2014; Kamphuis et al, 2015; see below)

Summary

Introduction

OVERVIEW Multiple sclerosis (MS) is a complex, debilitating, immunopathologic disease of the human central nervous system (CNS) characterized by chronic systemic inflammation, alterations in innate-immune signaling, progressive demyelination and axonal loss.

Results

Conclusion