Abstract

Multiple sclerosis (MS) belongs to demyelinating diseases, which are progressive and highly debilitating pathologies that imply a high burden both on individual patients and on society. Currently, several treatment strategies differ in the route of administration, adverse events, and possible risks. Side effects associated with multiple sclerosis medications range from mild symptoms, such as flu-like or irritation at the injection site, to serious ones, such as progressive multifocal leukoencephalopathy and other life-threatening events. Moreover, the agents so far available have proved incapable of fully preventing disease progression, mostly during the phases that consist of continuous, accumulating disability. Thus, new treatment strategies, able to halt or even reverse disease progression and specific for targeting solely the pathways that contribute to the disease pathogenesis, are highly desirable. Here, we provide an overview of the recent literature about peptide-based systems tested on experimental autoimmune encephalitis (EAE) models. Since peptides are considered a unique therapeutic niche and important elements in the pharmaceutical landscape, they could open up new therapeutic opportunities for the treatment of MS.

Highlights

  • Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that leads to progressive neurodegeneration

  • A crux of the disease is an autoimmune attack of the self-antigens, that is the proteins of the myelin sheath that wrap around the nerve fibers are mistaken for foreign agents by macrophages, CD4+ T, CD8+ T, and B cells infiltrating the blood-brain barrier (BBB)

  • Multiple sclerosis is divided into four types, named according to the way the disease acts on the body over time: Progressive Relapsing MS (PRMS), characterized by a steady degeneration since onset with super-imposed attacks, Relapsing-Remitting MS (RRMS), the most common disease course diagnosed for 85% of people, characterized by defined attacks of new or even increasing neurological symptoms, followed by periods of partial or complete recovery, Primary Progressive MS (PPMS), consisting of progressive disability from the onset of symptoms, and Secondary Progressive MS (SPMS), marked by an initial relapsing-remitting course that suddenly begins to progressively decline over time [7,8]

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Summary

Introduction

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that leads to progressive neurodegeneration. It is estimated that worldwide, more than 2.3 million people between ages 20 to 50 are affected by MS, that is usually diagnosed with signs and symptoms that may differ from person to person and throughout the disease, such as loss of balance and coordination, visual and sensory deficiency, fatigue, weakness, vertigo, pain, and cognitive difficulties [6]. Before being officially diagnosed with MS, patients can experience a first neurologic event indicative of potential MS, defined as Clinically Isolated Syndrome, that lasts for at least 24 h with symptoms and signs indicating either a single lesion (monofocal) or more than one lesion (multifocal) within the CNS. Multiple sclerosis is divided into four types, named according to the way the disease acts on the body over time: Progressive Relapsing MS (PRMS), characterized by a steady degeneration since onset with super-imposed attacks, Relapsing-Remitting MS (RRMS), the most common disease course diagnosed for 85% of people, characterized by defined attacks of new or even increasing neurological symptoms (relapses), followed by periods of partial or complete recovery (remissions), Primary Progressive MS (PPMS), consisting of progressive disability from the onset of symptoms, and Secondary Progressive MS (SPMS), marked by an initial relapsing-remitting course that suddenly begins to progressively decline over time [7,8]

Immunopathogenesis of MS
Current Available Therapeutic Approaches
Peptides Modulating T Cells’ Functions
Myelin-Based Autoantigen Peptides
Peptides Modulating Th Cell Subsets
Peptides Modulating Other Cells besides T Lymphocytes
Remyelination-Enhancing Peptide
Peptide Inhibiting Microglia Activation: γ377–395
Peptide
Findings
Conclusion

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