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Special Issue "Molecular Mechanisms in Demyelinating Disorders of the Central Nervous System"

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 30 September 2023 | Viewed by 7685

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Special Issue Editor

Dr. Paschalis Theotokis

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Guest Editor

1. Laboratory of Experimental Neurology and Neuroimmunology, 2nd Department of Neurology, AHEPA University Hospital, Thessaloniki, Greece
2. Laboratory of Histology and Embryology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece
Interests: neuroscience; multiple sclerosis; experimental autoimmune encephalomyelitis; intrathecal transplantation; stem cell differentiation; immunohistopathology; in situ hybridization; electron microscopy
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Special Issue Information

Dear Colleagues,

A demyelinating disease is a pathological condition of the nervous system that negatively affects the structure and function of the lipid sheath that surround axons, ultimately interfering with the nerve conduction. These lipid sheaths are lamellar membrane extensions of oligodendrocytes (OLs) in the central nervous system (CNS) and the Schwann cells in the peripheral nervous system (PNS). Myelinoclastic and leukodystrophic are the two categories into which demyelinating diseases have historically been divided. A typical, healthy myelin sheath is damaged in the first group as a result of a toxic, chemical, or autoimmune agent while genetic-based aberrant myelin that is degenerated is present in the latter one, better known as dysmyelination.

Among the three main inflammatory-based CNS demyelinating diseases are multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD) and acute disseminated encephalomyelitis (ADEM). MS is the most prevalent one, affecting millions of people worldwide. Since etiology of these diseases is still largely unknown, there’s a need to establish new biomarkers and prioritize the development of experimental research, particularly in the molecular level. I hereby invite authors to submit original research, review articles or commentaries on molecular mechanisms that shed light to therapeutic strategies in demyelinating disorders of the CNS.

Dr. Paschalis Theotokis
Guest Editor

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

demyelination
molecular mechanisms
oligodendrocyte precursor cells
myelinogenesis
dysmyelination
lipid metabolism
microglia and macrophages
experimental autoimmune
encephalomyelitis
biomarkers
remyelination

Published Papers (6 papers)

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Research

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Open AccessArticle

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses

Azita Soltanmohammadi

Simin Zargarani

Aleksandr Kamyshnyi

and

Valentyn Oksenych

Curr. Issues Mol. Biol. 2022, 44(11), 5728-5740; https://doi.org/10.3390/cimb44110388 - 18 Nov 2022

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Abstract

Multiple Sclerosis (MS) is a demyelinating autoimmune disorder of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) has been widely used to determine the pathogenesis of the disease and evaluate new treatment strategies for MS. Therefore, we investigated the efficacy of oral administration of a Myelin Oligodendrocyte Glycoprotein (MOG) in the treatment of EAE. Female C57BL/6 mice were utilized in three groups (Control group, received PBS orally; prevention group, oral administration of MOG_35–55 two weeks before EAE induction; treatment group, oral administration of MOG_35–55 after EAE induction). MOG administration, both as prevention and treatment, significantly controlled clinical score, weight loss, CNS inflammation, and demyelination, mainly through the modulation of T cell proliferation, and reduction in pro-inflammatory cytokines and transcription factors, including TNF-α, IFN-γ, IL-17, T-bet, and ROR-γt. MOG administration, both as prevention and treatment, also induced anti-inflammatory cytokines and transcription factors, including IL-4, TGF-β, GATA-3, and Foxp3. The results showed that oral administration of MOG, both as prevention and treatment, could efficiently control EAE development. Immunomodulatory mechanisms include the induction of Th2 and Treg cells and the suppression of pro-inflammatory Th1 and Th17 cells. Full article

(This article belongs to the Special Issue Molecular Mechanisms in Demyelinating Disorders of the Central Nervous System)

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Open AccessArticle

Pro-Inflammatory and Pro-Apoptotic Effects of the Non-Protein Amino Acid L-Azetidine-2-Carboxylic Acid in BV2 Microglial Cells

and

Curr. Issues Mol. Biol. 2022, 44(10), 4500-4516; https://doi.org/10.3390/cimb44100308 - 28 Sep 2022

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Abstract

L-Azetidine-2-carboxylic acid (AZE) is a toxic non-protein coding amino acid (npAA) that is highly abundant in sugar and table beets. Due to its structural similarity with the amino acid L-proline, AZE can evade the editing process during protein assembly in eukaryotic cells and be misincorporated into L-proline-rich proteins, potentially causing protein misfolding and other detrimental effects to cells. In this study, we sought to determine if AZE treatment triggered pro-inflammatory and pro-apoptotic responses in BV2 microglial cells. BV2 microglial cells exposed to AZE at increasing concentrations (0–2000 µM) at 0, 3, 6, 12 and 24 h were assayed for cell viability (MTT) and nitric oxide release (Griess assay). Annexin V-FITC/propidium iodide (PI) staining was used to assess apoptosis. Real-time qPCR, Western blot and immunocytochemistry were used to interrogate relevant pro- and anti-inflammatory and other molecular targets of cell survival response. AZE (at concentrations > 1000 µM) significantly reduced cell viability, increased BAX/Bcl2 ratio and caused cell death. Results were mirrored by a robust increase in nitric oxide release, percentage of activated/polarised cells and expression of pro-inflammatory markers (IL-1β, IL-6, NOS2, CD68 and MHC-2a). Additionally, we found that AZE induced the expression of the extracellular matrix degrading enzyme matrix metalloproteinase 9 (MMP-9) and brain derived neurotrophic factor (BDNF), two critical regulators of microglial motility and structural plasticity. Collectively, these data indicate that AZE-induced toxicity is associated with increased pro-inflammatory activity and reduced survival in BV2 microglia. This evidence may prompt for an increased monitoring of AZE consumption by humans. Full article

(This article belongs to the Special Issue Molecular Mechanisms in Demyelinating Disorders of the Central Nervous System)

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Open AccessArticle

Basic Analysis of the Cerebrospinal Fluid: An Important Framework for Laboratory Diagnostics of the Impairment of the Central Nervous System

and

Curr. Issues Mol. Biol. 2022, 44(8), 3666-3680; https://doi.org/10.3390/cimb44080251 - 14 Aug 2022

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Abstract

Laboratory analysis of basic cerebrospinal fluid (CSF) parameters is considered as essential for any CSF evaluation. It can provide rapidly very valuable information about the status of the central nervous system (CNS). Our retrospective study evaluated parameters of basic CSF analysis in cases of either infectious or non-infectious CNS involvement. Neutrophils are effector cells of innate immunity. Predominance of neutrophils was found in 98.2% of patients with purulent inflammation in CNS. Lymphocytes are cellular substrate of adaptive immunity. We found their predominance in 94.8% of patients with multiple sclerosis (MS), 66.7% of patients with tick-borne encephalitis (TBE), 92.2% of patients with neuroborreliosis, 83.3% of patients with inflammatory response with oxidative burst of macrophages in CNS and 75.0% of patients with malignant infiltration of meninges (MIM). The simultaneous assessment of aerobic and anaerobic metabolism in CSF using the coefficient of energy balance (KEB) allows us to specify the type of inflammation in CNS. We found predominantly aerobic metabolism (KEB > 28.0) in 100.0% CSF of patients with normal CSF findings and in 92.8% CSF of patients with MS. Predominant faintly anaerobic metabolism (28.0 > KEB > 20.0) in CSF was found in 71.8% patients with TBE and in 64.7% patients with neuroborreliosis. Strong anaerobic metabolism (KEB < 10.0) was found in the CSF of 99.1% patients with purulent inflammation, 100.0% patients with inflammatory response with oxidative burst of macrophages and in 80.6% patients with MIM. Joint evaluation of basic CSF parameters provides sufficient information about the immune response in the CSF compartment for rapid and reliable diagnosis of CNS involvement. Full article

(This article belongs to the Special Issue Molecular Mechanisms in Demyelinating Disorders of the Central Nervous System)

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Review

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Open AccessReview

Multiple Sclerosis: Inflammatory and Neuroglial Aspects

Giulio Papiri

Giordano D’Andreamatteo

and

Curr. Issues Mol. Biol. 2023, 45(2), 1443-1470; https://doi.org/10.3390/cimb45020094 - 08 Feb 2023

Viewed by 475

Abstract

Multiple sclerosis (MS) represents the most common acquired demyelinating disorder of the central nervous system (CNS). Its pathogenesis, in parallel with the well-established role of mechanisms pertaining to autoimmunity, involves several key functions of immune, glial and nerve cells. The disease’s natural history is complex, heterogeneous and may evolve over a relapsing-remitting (RRMS) or progressive (PPMS/SPMS) course. Acute inflammation, driven by infiltration of peripheral cells in the CNS, is thought to be the most relevant process during the earliest phases and in RRMS, while disruption in glial and neural cells of pathways pertaining to energy metabolism, survival cascades, synaptic and ionic homeostasis are thought to be mostly relevant in long-standing disease, such as in progressive forms. In this complex scenario, many mechanisms originally thought to be distinctive of neurodegenerative disorders are being increasingly recognized as crucial from the beginning of the disease. The present review aims at highlighting mechanisms in common between MS, autoimmune diseases and biology of neurodegenerative disorders. In fact, there is an unmet need to explore new targets that might be involved as master regulators of autoimmunity, inflammation and survival of nerve cells. Full article

(This article belongs to the Special Issue Molecular Mechanisms in Demyelinating Disorders of the Central Nervous System)

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Open AccessReview

Optic Neuritis in Multiple Sclerosis—A Review of Molecular Mechanisms Involved in the Degenerative Process

Manuela Andreea Ciapă

Delia Lidia Șalaru

Cristian Stătescu

Radu Andy Sascău

and

Camelia Margareta Bogdănici

Curr. Issues Mol. Biol. 2022, 44(9), 3959-3979; https://doi.org/10.3390/cimb44090272 - 02 Sep 2022

Viewed by 1090

Abstract

Multiple sclerosis is a central nervous system inflammatory demyelinating disease with a wide range of clinical symptoms, ocular involvement being frequently marked by the presence of optic neuritis (ON). The emergence and progression of ON in multiple sclerosis is based on various pathophysiological mechanisms, disease progression being secondary to inflammation, demyelination, or axonal degeneration. Early identification of changes associated with axonal degeneration or further investigation of the molecular processes underlying remyelination are current concerns of researchers in the field in view of the associated therapeutic potential. This article aims to review and summarize the scientific literature related to the main molecular mechanisms involved in defining ON as well as to analyze existing data in the literature on remyelination strategies in ON and their impact on long-term prognosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms in Demyelinating Disorders of the Central Nervous System)

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Open AccessReview

Developmental Cues and Molecular Drivers in Myelinogenesis: Revisiting Early Life to Re-Evaluate the Integrity of CNS Myelin

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Curr. Issues Mol. Biol. 2022, 44(7), 3208-3237; https://doi.org/10.3390/cimb44070222 - 19 Jul 2022

Cited by 2 | Viewed by 1866

Abstract

The mammalian central nervous system (CNS) coordinates its communication through saltatory conduction, facilitated by myelin-forming oligodendrocytes (OLs). Despite the fact that neurogenesis from stem cell niches has caught the majority of attention in recent years, oligodendrogenesis and, more specifically, the molecular underpinnings behind OL-dependent myelinogenesis, remain largely unknown. In this comprehensive review, we determine the developmental cues and molecular drivers which regulate normal myelination both at the prenatal and postnatal periods. We have indexed the individual stages of myelinogenesis sequentially; from the initiation of oligodendrocyte precursor cells, including migration and proliferation, to first contact with the axon that enlists positive and negative regulators for myelination, until the ultimate maintenance of the axon ensheathment and myelin growth. Here, we highlight multiple developmental pathways that are key to successful myelin formation and define the molecular pathways that can potentially be targets for pharmacological interventions in a variety of neurological disorders that exhibit demyelination. Full article

(This article belongs to the Special Issue Molecular Mechanisms in Demyelinating Disorders of the Central Nervous System)

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