Abstract
Multiple sclerosis (MS) is an autoimmune disorder characterised by demyelination of central nervous system neurons with subsequent damage, cell death and disability. While mechanisms exist in the CNS to repair this damage, they are disrupted in MS and currently there are no treatments to address this deficit. In recent years, increasing attention has been paid to the influence of the small, non-coding RNA molecules, microRNAs (miRNAs), in autoimmune disorders, including MS. In this review, we examine the role of miRNAs in remyelination in the different cell types that contribute to MS. We focus on key miRNAs that have a central role in mediating the repair process, along with several more that play either secondary or inhibitory roles in one or more aspects. Finally, we consider the current state of miRNAs as therapeutic targets in MS, acknowledging current challenges and potential strategies to overcome them in developing effective novel therapeutics to enhance repair mechanisms in MS.
Highlights
Multiple sclerosis (MS) is an autoimmune disorder characterized by an attack on central nervous system (CNS) myelin sheath and subsequent demyelination, resulting in axonal damage, neuronal loss and the formation of numerous localized sclerotic lesions [1]
We describe the specific role of miRNAs in remyelination in each major cell type involved in the process
The characteristic demyelination that occurs in MS leads to disease symptoms because of the disruption this causes to neuronal function—demyelinated axons are less efficient at transmitting electrical signals, and become vulnerable to more severe damage and even cell death [102,103]
Summary
Multiple sclerosis (MS) is an autoimmune disorder characterized by an attack on central nervous system (CNS) myelin sheath and subsequent demyelination, resulting in axonal damage, neuronal loss and the formation of numerous localized sclerotic lesions [1]. In PPMS, this phase of the disease appears from the onset, with no periods of remission and a steady accumulation of disability. This form of the disease affects approximately 15% of patients from the point of diagnosis [5]. While treatments for MS are available, they tend to focus on limiting immune activity and infiltration, leading to less inflammatory damage to the CNS, and so primarily have efficacy in RRMS patients. There is a relative lack of treatments that target the progressive phases of the disorder and focus on repairing damaged lesions [7] For this reason, understanding the biological processes that underlie myelin repair—remyelination—has become a research goal of considerable interest
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