scholarly journals Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

2020 ◽  
Vol 10 (9) ◽  
pp. 637
Author(s):  
Ekaterina Dubchenko ◽  
Alexander Ivanov ◽  
Natalia Spirina ◽  
Nina Smirnova ◽  
Mikhail Melnikov ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Endothelial Dysfunction ◽  
Pleiotropic Effect ◽  
Important Condition ◽  
Leading Role ◽  
The Central Nervous System ◽  
Ms Pathogenesis

Endothelial dysfunction is recognized as one of the leading factors in the pathogenesis of diseases of the central nervous system of various etiologies. Numerous studies have shown the role of hyperhomocysteinemia in the development of endothelial dysfunction and the prothrombogenic state. The most important condition in the development of multiple sclerosis (MS) is a dysregulation of the blood-brain barrier (BBB) and transendothelial leukocyte migration. It has been proven that homocysteine also contributes to the damage of neurons by the mechanism of excitotoxicity and the induction of the apoptosis of neurons. These processes can be one of the factors of neurodegenerative brain damage, which plays a leading role in the progression of MS. This review describes the pleiotropic effect of homocysteine on these processes and its role in MS pathogenesis.

scholarly journals miRNAs in Microglia: Important Players in Multiple Sclerosis Pathology

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142098118
Author(s):  
Alexander D. Walsh ◽  
Linda T. Nguyen ◽  
Michele D. Binder
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Approaches ◽  
Ribonucleic Acids ◽  
Microglial Phagocytosis ◽  
The Central Nervous System ◽  
And Function ◽  
Ms Pathogenesis

Microglia are the resident immune cells of the central nervous system and important regulators of brain homeostasis. Central to this role is a dynamic phenotypic plasticity that enables microglia to respond to environmental and pathological stimuli. Importantly, different microglial phenotypes can be both beneficial and detrimental to central nervous system health. Chronically activated inflammatory microglia are a hallmark of neurodegeneration, including the autoimmune disease multiple sclerosis (MS). By contrast, microglial phagocytosis of myelin debris is essential for resolving inflammation and promoting remyelination. As such, microglia are being explored as a potential therapeutic target for MS. MicroRNAs (miRNAs) are short non-coding ribonucleic acids that regulate gene expression and act as master regulators of cellular phenotype and function. Dysregulation of certain miRNAs can aberrantly activate and promote specific polarisation states in microglia to modulate their activity in inflammation and neurodegeneration. In addition, miRNA dysregulation is implicated in MS pathogenesis, with circulating biomarkers and lesion specific miRNAs identified as regulators of inflammation and myelination. However, the role of miRNAs in microglia that specifically contribute to MS progression are still largely unknown. miRNAs are being explored as therapeutic agents, providing an opportunity to modulate microglial function in neurodegenerative diseases such as MS. This review will focus firstly on elucidating the complex role of microglia in MS pathogenesis. Secondly, we explore the essential roles of miRNAs in microglial function. Finally, we focus on miRNAs that are implicated in microglial processes that contribute directly to MS pathology, prioritising targets that could inform novel therapeutic approaches to MS.

Role of inflammation and apoptosis in multiple sclerosis: Comparative analysis between the periphery and the central nervous system

2015 ◽  
Vol 287 ◽  
pp. 80-87 ◽  
Author(s):  
Beatrice Macchi ◽  
Francesca Marino-Merlo ◽  
Ugo Nocentini ◽  
Valerio Pisani ◽  
Salvatore Cuzzocrea ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Comparative Analysis ◽  
The Central Nervous System

scholarly journals Traditional Uses of Cannabinoids and New Perspectives in the Treatment of Multiple Sclerosis

Medicines ◽  
2018 ◽  
Vol 5 (3) ◽  
pp. 91 ◽  
Author(s):  
Francesca Gado ◽  
Maria Digiacomo ◽  
Marco Macchia ◽  
Simone Bertini ◽  
Clementina Manera
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Disease Progression ◽  
Endocannabinoid System ◽  
Neuroprotective Effects ◽  
Demyelinating Disorder ◽  
Immune Mediated ◽  
The Central Nervous System

Recent findings highlight the emerging role of the endocannabinoid system in the control of symptoms and disease progression in multiple sclerosis (MS). MS is a chronic, immune-mediated, demyelinating disorder of the central nervous system with no cure so far. It is widely reported in the literature that cannabinoids might be used to control MS symptoms and that they also might exert neuroprotective effects and slow down disease progression. This review aims to give an overview of the principal cannabinoids (synthetic and endogenous) used for the symptomatic amelioration of MS and their beneficial outcomes, providing new potentially possible perspectives for the treatment of this disease.

scholarly journals CD226 Gly307Ser Association With Neuromyelitis Optica in Southern Han Chinese

2012 ◽  
Vol 39 (4) ◽  
pp. 488-490 ◽  
Author(s):  
Chao Liu ◽  
Guansan Wang ◽  
Hong Liu ◽  
Yue Li ◽  
Jin Li ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Autoimmune Diseases ◽  
Neuromyelitis Optica ◽  
Han Chinese ◽  
Relapsing Remitting ◽  
The Central Nervous System ◽  
Relapsing Remitting Multiple Sclerosis

Background:Neuromyelitis optica (NMO) and multiple sclerosis (MS) are autoimmune diseases of the central nervous system with complex pathogeneses. NMO was once considered to be a severe variant of MS. There has been more evidence that a non-synonymous exchange (rs763361/Gly307Ser) in the gene for CD226 is linked to several autoimmune diseases including multiple sclerosis (MS). However, no studies have investigated the role of rs763361 in the pathogenesis of NMO.Objectives:The goal of our study is to evaluate the role of CD226 Gly307Ser in neuromyelitis optica (NMO) in Southern Han Chinese.Methods:Eight-nine NMO patients, 93 relapsing-remitting multiple sclerosis (RRMS) patients, and 122 controls (CTLs) were enrolled. The rs763361 alleles of the subjects were determined by sequencing-based typing.Results:The results strongly support that the TT genotypes are associated with NMO but are not significantly correlated with susceptibility for MS.Conclusions:CD226 Gly307Ser may correlate with risk of NMO in Southern Han Chinese.

Role of Prostaglandins in Multiple Sclerosis

2020 ◽  
Vol 26 (7) ◽  
pp. 730-742
Author(s):  
Surendra Gulla ◽  
Dakshayani Lomada ◽  
Anusha Lade ◽  
Reddanna Pallu ◽  
Madhava C. Reddy
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Disorders ◽  
Cognitive Disability ◽  
Demyelinating Disorder ◽  
Mediators Of Inflammation ◽  
The Central Nervous System ◽  
Lateral Sclerosis

: Multiple sclerosis (MS) is an autoimmune demyelinating disorder with chronic inflammation in the central nervous system, manifested by both physical and cognitive disability. Neuroinflammation and neurodegeneration are the phenomena that appear in the central nervous system associated with various neurodegenerative disorders, including MS, Alzheimer’s diseases, amyotrophic lateral sclerosis and Parkinson’s disease. Prostaglandins are one of the major mediators of inflammation that exhibit an important function in enhancing neuroinflammatory and neurodegenerative processes. These mediators would help understand the pathophysiology of MS as the combination of antagonists or agonists of prostaglandins receptors could be beneficial during the treatment of MS. The present review focuses on the role played by different prostaglandins and the enzymes which produced them in the etiopathogenesis of MS.

Denial of compensation for patients who developed multiple sclerosis or have existing disease made worse following acute stress or trauma

2012 ◽  
Vol 12 (3-4) ◽  
pp. 235-248
Author(s):  
Peter Oliver Behan ◽  
Abhijit Chaudhuri ◽  
Simone Hutchinson
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Acute Stress ◽  
Molecular Medicine ◽  
Future Research ◽  
Pathological Feature ◽  
The Central Nervous System ◽  
Prevailing View

An important legal question is the role of acute trauma on the central nervous system with stress in precipitating or worsening multiple sclerosis (MS). At present, the prevailing view in neurology is that there is no relationship. We show here that this opinion needs to be reappraised. Medicolegal decisions for compensation in court have hinged on this question, as do the future research and treatment. A critical analysis of highly important but hitherto neglected articles shows the prevailing view to be gravely mistaken. Modern molecular medicine has shown conclusively that trauma and stress (either alone or together) to the central nervous system cause disruption of the blood–brain barrier (BBB). Disruption of this BBB, a complex molecular process, is the basic pathological feature of MS and is affected in both trauma and stress. Its further study should lead to a rational mode of therapy and resolve the legal quagmire.

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