Remyelination in multiple sclerosis: realizing a long-standing challenge

Aharoni, Rina

doi:10.1586/14737175.2015.1112740

Cited by 5 publications

(1 citation statement)

References 23 publications

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“…GA increases neurotrophic factors such as brainderived neurotrophic factor, involved in neuronal and glial cell survival, and it may mediate neuroprotection. In addition, GA induces remyelination and enhances neurogenesis [16].…”

Section: Introductionmentioning

confidence: 99%

Beneficial Effect of Melatonin Alone or in Combination with Glatiramer Acetate and Interferon β-1b on Experimental Autoimmune Encephalomyelitis

et al. 2022

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Experimental autoimmune encephalomyelitis (EAE) is a relevant animal model of multiple sclerosis (MS). Oxidative stress and chronic inflammation play a major role in the pathogenesis of MS and EAE. Melatonin, a neurohormone, has potent anti-inflammatory properties. The aim of our study was to assess the therapeutic properties of melatonin alone or in combination with interferon β-1b (IFNβ-1b) or glatiramer acetate (GA) on EAE. EAE was induced in male Sprague-Dawley rats with an intraperitoneal injection of a homogenate of spinal cord and pig brain. At day 10 post immunization, rats were euthanized, and their brains were immediately excised and processed to measure oxidative stress markers and membrane fluidity. In addition, proinflammatory cytokines were quantified in plasma. Melatonin alone or in combination with GA and IFNβ-1b inhibited the disease process of EAE and the synthesis of proinflammatory cytokines, caused a significant decrement in oxidative stress markers, and preserved the membrane fluidity in the motor cortex, midbrain, and spinal cord. The cumulative index score was significantly reduced in EAE rats treated with melatonin alone or in combination with GA and IFNβ-1b. In conclusion, our findings provide preclinical evidence for the use of melatonin as an adjuvant therapeutic treatment for MS.

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Section: Introductionmentioning

confidence: 99%

Beneficial Effect of Melatonin Alone or in Combination with Glatiramer Acetate and Interferon β-1b on Experimental Autoimmune Encephalomyelitis

et al. 2022

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Role of Oligodendrocyte Dysfunction in Demyelination, Remyelination and Neurodegeneration in Multiple Sclerosis

Dulamea

2017

Advances in Experimental Medicine and Biology

105

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Oligodendrocytes (OLs) are the myelinating cells of the central nervous system (CNS) during development and throughout adulthood. They result from a complex and well controlled process of activation, proliferation, migration and differentiation of oligodendrocyte progenitor cells (OPCs) from the germinative niches of the CNS. In multiple sclerosis (MS), the complex pathological process produces dysfunction and apoptosis of OLs leading to demyelination and neurodegeneration. This review attempts to describe the patterns of demyelination in MS, the steps involved in oligodendrogenesis and myelination in healthy CNS, the different pathways leading to OLs and myelin loss in MS, as well as principles involved in restoration of myelin sheaths. Environmental factors and their impact on OLs and pathological mechanisms of MS are also discussed. Finally, we will present evidence about the potential therapeutic targets in re-myelination processes that can be accessed in order to develop regenerative therapies for MS.

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Effect of Etazolate upon Cuprizone-induced Demyelination In Vivo: Behavioral and Myelin Gene Analysis

et al. 2021

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Remyelination in multiple sclerosis: realizing a long-standing challenge

Cited by 5 publications

References 23 publications

Beneficial Effect of Melatonin Alone or in Combination with Glatiramer Acetate and Interferon β-1b on Experimental Autoimmune Encephalomyelitis

Beneficial Effect of Melatonin Alone or in Combination with Glatiramer Acetate and Interferon β-1b on Experimental Autoimmune Encephalomyelitis

Role of Oligodendrocyte Dysfunction in Demyelination, Remyelination and Neurodegeneration in Multiple Sclerosis

Effect of Etazolate upon Cuprizone-induced Demyelination In Vivo: Behavioral and Myelin Gene Analysis

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