What Is The Function Of Myelin In The Nervous System – JAK2 phosphorylation signals and related cytokines involved in chronic rhinosinusitis with nasal polyps and correlated with disease severity

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What Is The Function Of Myelin In The Nervous System

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By Ilias Kalafatakis Ilias Kalafatakis Scilit Preprints.org Google Scholar 1, 2 and Domna Karagogeos Domna Karagogeos Scilit Preprints.org Google Scholar 1, 2, *

What Is A Neuron? Diagrams, Types, Function, And More

Received: 30 May 2021 / Revised: 16 July 2021 / Accepted: 16 July 2021 / Published: 20 July 2021

Oligodendrocytes, the myelin-producing cells of the CNS, regulate the complex process of myelination under physiological and pathological conditions, greatly assisted by other types of glial cells, such as microglia, the brain’s resident macrophage-like innate immune cells. In this review, we summarize how oligodendrocytes orchestrate myelination and especially myelin repair after injury and present novel aspects of oligodendroglial functions. We highlight the contribution of microglia in myelin generation and regeneration, discussing their beneficial and detrimental roles, particularly in remyelination, highlighting the cellular and molecular components involved. Finally, we present recent findings towards preclinical human stem cell-derived models for studying microglia in human pathologies and the role of the microbiome on glial cell functions.

The myelin sheath is the membranous structure that surrounds most of the axons of the central (CNS) and peripheral (PNS) nervous systems of vertebrates. This is an evolutionary adaptation that allows rapid signal propagation over greater distances, a feature of increasing animal body size. Myelin is produced by a myelinating glial cell, an oligodendrocyte in the CNS, and a Schwann cell in the PNS, spirally arranged around the axon in a compact sheath. Signal conduction is optimal due to the increase in resistance and the decrease in membrane capacitance of axons, which increases the speed of propagation of the action potential up to tenfold [1, 2].

In addition to this important insulating function, myelin assumes several critical functions in the nervous system. It mechanically protects axons by isolating the electrical signal from the microenvironment. Importantly, oligodendrocytes have been shown to provide metabolic support to neurons and regulate ion and water homeostasis [ 3 , 4 , 5 , 6 ]. Oligodendrocytes have recently been appreciated to influence neuronal circuits by being able to respond to activity-dependent changes by regulating myelin production [ 7 , 8 , 9 , 10 ]. Indeed, our understanding of the events leading to myelin production has been enriched by recently identified regulatory factors that control various aspects of glial development and by large-scale analysis showing a wide variety and complexity of progenitor and mature cells involved in myelination, a process , which is considered active throughout the life of the organism.

Role Of Connexin Based Gap Junction Channels In Communication Of Myelin Sheath In Schwann Cells

The regulation of myelination, either during development or during recovery or adaptive conditions, is mediated by complex interactions between neurons and glia. In particular, all types of glial cells participate in not yet fully understood ways in myelin development and its modulation. In this review, we discuss essential aspects of the cross-talk between oligodendrocytes and another glial cell type, microglia, in maintaining myelin homeostasis and also explore how this cross-talk is affected under inflammatory conditions that often lead to myelin pathologies.

Myelinating oligodendrocytes originate from oligodendrocyte precursor cells (OPCs), which are highly proliferative cells derived in discrete waves during development. In the ventricular zone of the forebrain, for example, neuroepithelial progenitors generate OPCs from E12.5 until birth. OPCs are characterized by the expression of platelet-derived growth factor receptor A (PDGFR-a), neuron-glial antigen 2 (NG2) proteoglycan, and gangliosides recognized by the A2B5 antibody. Elegant studies on oligodendroglial development elucidated the mechanisms of specification and differentiation of OPCs towards the myelinating phenotype and showed that Shh-dependent (early phase) and independent (late phase) signaling as well as the expression of the transcription factors Olig1, Olig2, Mash, Nkx2.2 and Sox10 are essential in these processes. OPCs migrate while still proliferating to populate the CNS, differentiate to a premyelinating identity, and at this point are able to wrap around axons; however, they are still unable to form mature myelin, a step that occurs upon expression of myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG). Several key regulators of this journey have been identified, including morphogenic signaling (Shh, Wnt), as well as several transcription factors and miRNAs [ 11 , 12 , 13 ].

As myelin continues to be generated in the healthy adult CNS, at least two sources of OPCs have been revealed, namely the progenitors of the subventricular zone (SVZ) and the NG2+/PDGFRα+ cells distributed in the CNS. These cells maintain their proliferative capacity, so oligodendrocytes are continuously generated. Recent evidence points to the formation of new oligodendrocytes as an important process in myelin plasticity coupled with motor skill learning [14, 15].

Demyelination is defined as the loss of myelin around axons due to congenital conditions or damage to the CNS (such as inflammation or injury). The prototype demyelinating pathological entity is multiple sclerosis (MS), a chronic inflammatory disease causing focal destruction of the myelin sheath and glial scar. MS is the most common acquired CNS demyelinating disease of as yet unknown etiology. On brain magnetic resonance imaging (MRI), the pathologic hallmark of the disease appears as white matter plaques, which are hyperintense lesions widely scattered throughout the CNS, although the optic nerves, brainstem, spinal cord, and periventricular white matter are commonly affected places. The pathogenesis of MS is characterized by breakdown of the blood-brain barrier with subsequent active recruitment of immune cells and a cascade of pathologies that range from lymphocyte infiltration and microglial activation to myelin sheath breakdown and axonal degeneration [16, 17, 18]. .

Discovery Of The Function Of Myelinated Fibers In Conduction Followed…

In MS, a cascade of neuroinflammatory processes eventually leads to damage to myelinating oligodendrocytes, causing demyelination; although the initial damage leading to oligodendrocyte death and myelin loss remains elusive, these events may arise from infiltrating immune cells but also within the CNS itself [19].

It is generally accepted that prophagocytic activity precedes complete myelin phagocytosis. These early events show no evidence of oligodendrocyte apoptosis, pointing to alternative mechanisms of cell death. Microglia are seen in these early-stage lesions. Myelin phagocytosis is thought to arise from the action of myelin-specific T cells that have been activated by antigen-presenting cells (microglia and dendritic cells) and thus initiate the full inflammatory sequence of events. In the former resting inflammatory cascade, parenchymal microglia also participate by releasing cytokines such as interleukin 12 (IL-12) and IL-13, which enhance Th1 cell differentiation and myelin damage through the release of NO and glutamate. Using an inducible oligodendrocyte depletion model in adults, it was shown that oligodendrocyte loss is followed by CD4+ T cells leading to secondary demyelination [20]. Although some of the pathophysiological mechanisms and players responsible for CNS demyelination have been described [21], the full picture still needs to be elucidated. Thus, it is unclear whether oligodendrocyte damage is the root or the result of inflammation.

Several rodent models of demyelination exist. None is capable of recapitulating all aspects of human disease, but the most common patterns resemble distinct phases and stages of the condition (inflammatory, autoimmune, and demyelination-remyelination processes). In these models, demyelination is accomplished by stimulation of the immune system, local or systemic administration of toxins, genetically encoded expression of toxins, or viral transduction. Experimental autoimmune encephalomyelitis (EAE), the toxic cuprizone demyelination model, and the lysolecithin (LPC) model are among the most commonly used [22, 23].

Myelin repair occurs in the human CNS as well as in some rodent models of MS. Remyelinated axons have a characteristically thin myelin sheath and short internodes. However, there is extensive heterogeneity due to disease duration, stage and phenotype. It is currently unclear whether indeed, as some studies have shown, remyelination is more effective in early demyelinating lesions and then follows a declining course [24, 25]. Demyelinating disease progression has been observed to superimpose and overtake myelin repair, indicating a close interaction between the two processes [26], suggesting that myelin repair is

Aging Myelin: A New Perspective In Alzheimer’s Disease Progression

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