scholarly journals Role of Multifocal Visually Evoked Potential as a Biomarker of Demyelination, Spontaneous Remyelination, and Myelin Repair in Multiple Sclerosis

2021 ◽  
Vol 15 ◽  
Author(s):  
Alexandr Klistorner ◽  
Stuart L. Graham
Keyword(s):  
Multiple Sclerosis ◽  
Evoked Potential ◽  
Visual Stimulation ◽  
Visual Pathway ◽  
Event Related Potential ◽  
Current View ◽  
Myelin Repair ◽  
Visually Evoked Potential

Multiple sclerosis (MS) is a complex disease of the central nervous system (CNS), characterized by inflammation, demyelination, neuro-axonal loss, and gliosis. Inflammatory demyelinating lesions are a hallmark of the disease. Spontaneous remyelination, however, is often incomplete and strategies that promote remyelination are needed. As a result, accurate and sensitive in vivo measures of remyelination are necessary. The visual pathway provides a unique opportunity for in vivo assessment of myelin damage and repair in the MS-affected brain since it is highly susceptible to damage in MS and is a very frequent site of MS lesions. The visually evoked potential (VEP), an event-related potential generated by the striate cortex in response to visual stimulation, is uniquely placed to serve as a biomarker of the myelination along the visual pathway. The multifocal VEP (mfVEP) represents a most recent addition to the array of VEP stimulations. This article provides a current view on the role of mfVEP as a biomarker of demyelination, spontaneous remyelination, and myelin repair in MS.

scholarly journals The role of optical coherence tomography and infrared oculography in assessing the visual pathway and CNS in multiple sclerosis

2018 ◽  
Vol 8 (5) ◽  
pp. 323-335 ◽  
Author(s):  
Danko Coric ◽  
Jenny A Nij Bijvank ◽  
Laurentius J van Rijn ◽  
Axel Petzold ◽  
Lisanne J Balk
Keyword(s):  
Multiple Sclerosis ◽  
Optical Coherence Tomography ◽  
Visual Pathway ◽  
Optical Coherence

A Systematic Review on the Role of Arachidonic Acid Pathway in Multiple Sclerosis

2020 ◽  
Vol 19 ◽  
Author(s):  
Malvina Hoxha ◽  
Erila Spahiu ◽  
Emanuela Prendi ◽  
Bruno Zappacosta
Keyword(s):  
Multiple Sclerosis ◽  
Systematic Review ◽  
Arachidonic Acid ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Lox Inhibitors ◽  
Acid Pathway ◽  
Arachidonic Acid Pathway

Background & Objective: Multiple sclerosis (MS) is an inflammatory neurodegenerative disease characterized by destruction of oligodendrocytes, immune cell infiltration and demyelination. Inflammation plays a significant role in MS, and the inflammatory mediators such as eicosanoids, leukotrienes, superoxide radicals are involved in pro-inflammatory responses in MS. In this systematic review we tried to define and discuss all the findings of in vivo animal studies and human clinical trials on the potential association between arachidonic acid (AA) pathway and multiple sclerosis. Methods: A systematic literature search across Pubmed, Scopus, Embase and Cochrane database was conducted. This systematic review was performed according to PRISMA guidelines. Results: A total of 146 studies were included, of which 34 were conducted in animals, 58 in humans, and 60 studies reported the role of different compounds that target AA mediators or their corresponding enzymes/ receptors, and can have a therapeutic effect in MS. These results suggest that eicosanoids have significant roles in experimental autoimmune encephalomyelitis (EAE) and MS. The data from animal and human studies elucidated that PGI2, PGF2α, PGD2, isoprostanes, PGE2, PLA2, LTs are increased in MS. PLA2 inhibition modulates the progression of the disease. PGE1 analogues can be a useful option in the treatment of MS. Conclusions: All studies reported the beneficial effects of COX and LOX inhibitors in MS. The hybrid compounds, such as COX-2 inhibitors/TP antagonists and 5-LOX inhibitors can be an innovative approach for multiple sclerosis treatment. Future work in MS should shed light in synthesizing new compounds targeting arachidonic acid pathway.

scholarly journals Multiple Sclerosis CD49d+CD154+ As Myelin-Specific Lymphocytes Induced During Remyelination

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 15
Author(s):  
Paweł Piatek ◽  
Magdalena Namiecinska ◽  
Małgorzata Domowicz ◽  
Marek Wieczorek ◽  
Sylwia Michlewska ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cumulative Effect ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System ◽  
Cns Demyelination ◽  
The Brain ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system (CNS) mediated by autoreactive lymphocytes. The role of autoreactive lymphocytes in the CNS demyelination is well described, whereas very little is known about their role in remyelination during MS remission. In this study, we identified a new subpopulation of myelin-specific CD49d+CD154+ lymphocytes presented in the peripheral blood of MS patients during remission, that proliferated in vitro in response to myelin peptides. These lymphocytes possessed the unique ability to migrate towards maturing oligodendrocyte precursor cells (OPCs) and synthetize proinflammatory chemokines/cytokines. The co-culture of maturing OPCs with myelin-specific CD49d+CD154+ lymphocytes was characterized by the increase in proinflammatory chemokine/cytokine secretion that was not only a result of their cumulative effect of what OPCs and CD49d+CD154+ lymphocytes produced alone. Moreover, maturing OPCs exposed to exogenous myelin peptides managed to induce CD40-CD154-dependent CD49d+CD154+ lymphocyte proliferation. We confirmed, in vivo, the presence of CD49d+CD154+ cells close to maturating OPCs and remyelinating plaque during disease remission in the MS mouse model (C57Bl/6 mice immunized with MOG35-55) by immunohistochemistry. Three weeks after an acute phase of experimental autoimmune encephalomyelitis, CD49d+/CD154+ cells were found to be co-localized with O4+ cells (oligodendrocyte progenitors) in the areas of remyelination identified by myelin basic protein (MBP) labelling. These data suggested that myelin-specific CD49d+CD154+ lymphocytes present in the brain can interfere with remyelination mediated by oligodendrocytes probably as a result of establishing proinflammatory environment.

scholarly journals Advances in brain imaging in multiple sclerosis

2019 ◽  
Vol 12 ◽  
pp. 175628641985972 ◽  
Author(s):  
Rosa Cortese ◽  
Sara Collorone ◽  
Olga Ciccarelli ◽  
Ahmed T. Toosy
Keyword(s):  
Multiple Sclerosis ◽  
Brain Imaging ◽  
Imaging Techniques ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Disability Outcome ◽  
Magnetic Resonance Imaging Mri ◽  
Ms Pathogenesis

Brain imaging is increasingly used to support clinicians in diagnosing multiple sclerosis (MS) and monitoring its progression. However, the role of magnetic resonance imaging (MRI) in MS goes far beyond its clinical application. Indeed, advanced imaging techniques have helped to detect different components of MS pathogenesis in vivo, which is now considered a heterogeneous process characterized by widespread damage of the central nervous system, rather than multifocal demyelination of white matter. Recently, MRI biomarkers more sensitive to disease activity than clinical disability outcome measures, have been used to monitor response to anti-inflammatory agents in patients with relapsing–remitting MS. Similarly, MRI markers of neurodegeneration exhibit the potential as primary and secondary outcomes in clinical trials for progressive phenotypes. This review will summarize recent advances in brain neuroimaging in MS from the research setting to clinical applications.

scholarly journals The Role of Molecular Imaging as a Marker of Remyelination and Repair in Multiple Sclerosis

2021 ◽  
Vol 23 (1) ◽  
pp. 474
Author(s):  
Ido Ben-Shalom ◽  
Arnon Karni ◽  
Hadar Kolb
Keyword(s):  
Multiple Sclerosis ◽  
Molecular Imaging ◽  
Disease Progression ◽  
Acute Inflammation ◽  
Imaging Biomarkers ◽  
Underlying Mechanisms

The appearance of new disease-modifying therapies in multiple sclerosis (MS) has revolutionized our ability to fight inflammatory relapses and has immensely improved patients’ quality of life. Although remarkable, this achievement has not carried over into reducing long-term disability. In MS, clinical disability progression can continue relentlessly irrespective of acute inflammation. This “silent” disease progression is the main contributor to long-term clinical disability in MS and results from chronic inflammation, neurodegeneration, and repair failure. Investigating silent disease progression and its underlying mechanisms is a challenge. Standard MRI excels in depicting acute inflammation but lacks the pathophysiological lens required for a more targeted exploration of molecular-based processes. Novel modalities that utilize nuclear magnetic resonance’s ability to display in vivo information on imaging look to bridge this gap. Displaying the CNS through a molecular prism is becoming an undeniable reality. This review will focus on “molecular imaging biomarkers” of disease progression, modalities that can harmoniously depict anatomy and pathophysiology, making them attractive candidates to become the first valid biomarkers of neuroprotection and remyelination.

scholarly journals In vivo conversion of astrocytes into oligodendrocyte lineage cells with transcription factor Sox10; Promise for myelin repair in multiple sclerosis

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0203785 ◽  
Author(s):  
Akram Mokhtarzadeh Khanghahi ◽  
Leila Satarian ◽  
Wenbin Deng ◽  
Hossein Baharvand ◽  
Mohammad Javan
Keyword(s):  
Multiple Sclerosis ◽  
Transcription Factor ◽  
Myelin Repair

scholarly journals Myelin repair: the role of stem and precursor cells in multiple sclerosis

2007 ◽  
Vol 363 (1489) ◽  
pp. 171-183 ◽  
Author(s):  
Siddharthan Chandran ◽  
David Hunt ◽  
Alexis Joannides ◽  
Chao Zhao ◽  
Alastair Compston ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Dominant Role ◽  
Experimental Studies ◽  
Precursor Cells ◽  
Potential Contribution ◽  
Myelin Repair ◽  
Relapsing Remitting ◽  
Clinical Biology ◽  
Progressive Stage

Multiple sclerosis is the most common potential cause of neurological disability in young adults. The disease has two distinct clinical phases, each reflecting a dominant role for separate pathological processes: inflammation drives activity during the relapsing–remitting stage and axon degeneration represents the principal substrate of progressive disability. Recent advances in disease-modifying treatments target only the inflammatory process. They are ineffective in the progressive stage, leaving the science of disease progression unsolved. Here, the requirement is for strategies that promote remyelination and prevent axonal loss. Pathological and experimental studies suggest that these processes are tightly linked, and that remyelination or myelin repair will both restore structure and protect axons. This review considers the basic and clinical biology of remyelination and the potential contribution of stem and precursor cells to enhance and supplement spontaneous remyelination.

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