scholarly journals New Insights into the Role of Oxidative Stress Mechanisms in the Pathophysiology and Treatment of Multiple Sclerosis

2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
Bożena Adamczyk ◽  
Monika Adamczyk-Sowa
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Chronic Phase ◽  
Current Treatment ◽  
New Drugs ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
The Brain ◽  
Methods Of Treatment

Multiple sclerosis (MS) is a multifactorial disease of the central nervous system (CNS) characterized by an inflammatory process and demyelination. The etiology of the disease is still not fully understood. Therefore, finding new etiological factors is of such crucial importance. It is suspected that the development of MS may be affected by oxidative stress (OS). In the acute phase OS initiates inflammatory processes and in the chronic phase it sustains neurodegeneration. Redox processes in MS are associated with mitochondrial dysfunction, dysregulation of axonal bioenergetics, iron accumulation in the brain, impaired oxidant/antioxidant balance, and OS memory. The present paper is a review of the current literature about the role of OS in MS and it focuses on all major aspects. The article explains the mechanisms of OS, reports unique biomarkers with regard to their clinical significance, and presents a poorly understood relationship between OS and neurodegeneration. It also provides novel methods of treatment, including the use of antioxidants and the role of antioxidants in neuroprotection. Furthermore, adding new drugs in the treatment of relapse may be useful. The article considers the significance of OS in the current treatment of MS patients.

scholarly journals A Review of Various Antioxidant Compounds and their Potential Utility as Complementary Therapy in Multiple Sclerosis

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1528 ◽  
Author(s):  
Elzbieta Dorota Miller ◽  
Angela Dziedzic ◽  
Joanna Saluk-Bijak ◽  
Michal Bijak
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Complex Disease ◽  
Early Stage ◽  
Symptomatic Treatment ◽  
Complementary Therapy ◽  
Antioxidant Compounds ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
Stress Mediators

Multiple sclerosis (MS) is a complex disease of the central nervous system (CNS). The etiology of this multifactorial disease has not been clearly defined. Conventional medical treatment of MS has progressed, but is still based on symptomatic treatment. One of the key factors in the pathogenesis of MS is oxidative stress, enhancing inflammation and neurodegeneration. In MS, both reactive oxygen and nitrogen species are formed in the CNS mainly by activated macrophages and microglia structures, which can lead to demyelination and axon disruption. The course of MS is associated with the secretion of many inflammatory and oxidative stress mediators, including cytokines (IL-1b, IL-6, IL-17, TNF-α, INF-γ) and chemokines (MIP-1a, MCP-1, IP10). The early stage of MS (RRMS) lasts about 10 years, and is dominated by inflammatory processes, whereas the chronic stage is associated with neurodegenerative axon and neuron loss. Since oxidative damage has been known to be involved in inflammatory and autoimmune-mediated processes, antioxidant therapy could contribute to the reduction or even prevention of the progression of MS. Further research is needed in order to establish new aims for novel treatment and provide possible benefits to MS patients. The present review examines the roles of oxidative stress and non-pharmacological anti-oxidative therapies in MS.

scholarly journals Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Genaro G. Ortiz ◽  
Fermín P. Pacheco-Moisés ◽  
Oscar K. Bitzer-Quintero ◽  
Ana C. Ramírez-Anguiano ◽  
Luis J. Flores-Alvarado ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Tissue Injury ◽  
Autoimmune Disorder ◽  
Demyelinating Lesions ◽  
The Central Nervous System ◽  
The Brain ◽  
And Oxidative Stress

Multiple sclerosis (MS) exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the blood-brain barrier (BBB), the recruitment of lymphocytes, microglia, and macrophages to lesion sites, the presence of multiple lesions, generally being more pronounced in the brain stem and spinal cord, the predominantly perivascular location of lesions, the temporal maturation of lesions from inflammation through demyelination, to gliosis and partial remyelination, and the presence of immunoglobulin in the central nervous system and cerebrospinal fluid. Lymphocytes activated in the periphery infiltrate the central nervous system to trigger a local immune response that ultimately damages myelin and axons. Pro-inflammatory cytokines amplify the inflammatory cascade by compromising the BBB, recruiting immune cells from the periphery, and activating resident microglia. inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in the demyelination and free radical-mediated tissue injury in the pathogenesis of MS. The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines which contribute to the development and progression of the disease. Inflammation can lead to oxidative stress and vice versa. Thus, oxidative stress and inflammation are involved in a self-perpetuating cycle.

scholarly journals The Contribution of Formyl Peptide Receptor Dysfunction to the Course of Neuroinflammation: A Potential Role in the Brain Pathology

2020 ◽  
Vol 18 (3) ◽  
pp. 229-249 ◽  
Author(s):  
Ewa Trojan ◽  
Natalia Bryniarska ◽  
Monika Leśkiewicz ◽  
Magdalena Regulska ◽  
Katarzyna Chamera ◽  
...  
Keyword(s):  
Potential Role ◽  
Membrane Receptors ◽  
Formyl Peptide Receptor ◽  
Proinflammatory Response ◽  
Formyl Peptide ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
G Protein Coupled ◽  
The Brain

: Chronic inflammatory processes within the central nervous system (CNS) are in part responsible for the development of neurodegenerative and psychiatric diseases. These processes are associated with, among other things, the increased and disturbed activation of microglia and the elevated production of proinflammatory factors. Recent studies indicated that the disruption of the process of resolution of inflammation (RoI) may be the cause of CNS disorders. It is shown that the RoI is regulated by endogenous molecules called specialized pro-resolving mediators (SPMs), which interact with specific membrane receptors. Some SPMs activate formyl peptide receptors (FPRs), which belong to the family of seven-transmembrane G protein-coupled receptors. These receptors take part not only in the proinflammatory response but also in the resolution of the inflammation process. Therefore, the activation of FPRs might have complex consequences. : This review discusses the potential role of FPRs, and in particular the role of FPR2 subtype, in the brain under physiological and pathological conditions and their involvement in processes underlying neurodegenerative and psychiatric disorders as well as ischemia, the pathogenesis of which involves the dysfunction of inflammatory processes.

scholarly journals The Role of Sex Hormones in Multiple Sclerosis

2018 ◽  
Vol 80 (1-2) ◽  
pp. 93-99 ◽  
Author(s):  
Mirla Avila ◽  
Arpana Bansal ◽  
John Culberson ◽  
Alan N. Peiris
Keyword(s):  
Multiple Sclerosis ◽  
Sex Hormones ◽  
Treatment Strategies ◽  
Female Gender ◽  
Current Treatment ◽  
Sex Hormone ◽  
Immune Mediated ◽  
Autoimmune Conditions ◽  
The Central Nervous System

Multiple sclerosis (MS) is a chronic inflammatory demyelination disorder with an immune-mediated pathophysiology that affects the central nervous system (CNS). Like other autoimmune conditions, it has a predilection for female gender. This suggests a gender bias and a possible hormonal association. Inflammation and demyelination are hallmarks of MS. Oligodendrocytes are the myelinating cells of the CNS and these continue to be generated by oligodendrocyte precursor cells (OPCs). The process of remyelination represents a major form of plasticity in the developing adult CNS. Remyelination does occur in MS, but the process is largely inadequate and/or incomplete. Current treatment strategies primarily focus on reducing inflammation or immunosuppression, but there is a need for more extensive research on re-myelination as a possible mechanism of treatment. Previous studies have shown that pregnancy leads to an increase in OPC proliferation, oligodendrocyte generation and the number of myelinated axons in the maternal CNS. Studies have also suggested that this remyelination is possibly mediated by estriol. Sex hormones in particular have been shown to have an immuno-protective effect in TH1-driven autoimmunity diseases. The aim of our article is to review the available research on sex hormone-specific immune modulatory effects, assess its remyelination potential in MS, and suggest a future path for more extensive research on sex hormone as a target for therapeutics in MS.

scholarly journals Shedding light on the role of CX3CR1 in the pathogenesis of schizophrenia

2021 ◽  
Author(s):  
Katarzyna Chamera ◽  
Magdalena Szuster-Głuszczak ◽  
Agnieszka Basta-Kaim
Keyword(s):  
Experimental Studies ◽  
Physiological Processes ◽  
Unique System ◽  
The Family ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
G Protein Coupled ◽  
The Brain ◽  
Brain Homeostasis

AbstractSchizophrenia has a complex and heterogeneous molecular and clinical picture. Over the years of research on this disease, many factors have been suggested to contribute to its pathogenesis. Recently, the inflammatory processes have gained particular interest in the context of schizophrenia due to the increasing evidence from epidemiological, clinical and experimental studies. Within the immunological component, special attention has been brought to chemokines and their receptors. Among them, CX3C chemokine receptor 1 (CX3CR1), which belongs to the family of seven-transmembrane G protein-coupled receptors, and its cognate ligand (CX3CL1) constitute a unique system in the central nervous system. In the view of regulation of the brain homeostasis through immune response, as well as control of microglia reactivity, the CX3CL1–CX3CR1 system may represent an attractive target for further research and schizophrenia treatment. In the review, we described the general characteristics of the CX3CL1–CX3CR1 axis and the involvement of this signaling pathway in the physiological processes whose disruptions are reported to participate in mechanisms underlying schizophrenia. Furthermore, based on the available clinical and experimental data, we presented a guide to understanding the implication of the CX3CL1–CX3CR1 dysfunctions in the course of schizophrenia.

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 Nutrientes y alimentos en la esclerosis múltiple

2020 ◽  
Vol 70 (1) ◽  
pp. 60-74
Author(s):  
Virginia Sedeño Monge ◽  
Eduardo A Fabre Palacios ◽  
Cristina López García ◽  
María de L Meza Jiménez
Keyword(s):  
Multiple Sclerosis ◽  
Vitamin D ◽  
Scientific Evidence ◽  
Short Chain Fatty Acids ◽  
Vitamina D ◽  
Esclerosis Múltiple ◽  
Increased Risk ◽  
Inflammatory Processes ◽  
The Central Nervous System

La alimentación influye en la mejora de la sintomatología de cualquier enfermedad, incluida la esclerosis múltiple (EM),la cual, se caracteriza por un proceso inflamatorio crónico, autoinmune del sistema nervioso central generando situaciones como inflamación, alteraciones; digestivas y mentales, discapacidad, y fatiga. El propósito de la presente revisión fue identificar la evidencia científica sobre los aspectos nutricionales que mejoran la progresión de EM. La metodología consistió en la búsqueda de literatura, en bases de datos electrónicas, referente a nutrición y esclerosis múltiple, principalmente entre los años 2015-2020. Entre los resultados de los aspectos nutricionales que mostraron eficacia en mejorar la progresión de EM, se encuentran el zinc, vitamina D, fibra, probióticos, aceite de pescado y de oliva, cacao, cúrcuma, y salmón. Existen evidencias del papel inmunomodulador del Zn y de la vitamina D en la inhibición de la producción de citocinas proinflamatorias. Niveles bajos de ambos componentes se asocian con mayor riesgo de padecer EM. Otros componentes de interés nutricional son la fibra y probióticos; producen ácidos grasos de cadena corta, con propiedades antiinflamatorias. La primera se conoce por su papel en la motilidad gastrointestinal y los segundos por su acción celular y molecular en procesos inflamatorios, y modulación del microbioma, por mencionar algunos. Los aspectos nutricionales antes mencionados pueden contribuir a modular la inflamación y mejorar la fatiga. Finalmente, este documento genera un panorama importante para continuar con la investigación referente a la influencia de la alimentación en pacientes con EM. Diet influences the improvement of the symptoms of any disease, including multiple sclerosis (MS), which is characterized by a chronic, autoimmune inflammatory process of the central nervous system generating situations such as inflammation, mental and digestive alterations, disability and fatigue. The aim of this review was to identify the scientific evidence on the nutritional aspects that improve the progression of MS. The methodology consisted of searching literature, in electronic databases, referring to nutrition and multiple sclerosis, mainly between the years 2015-2020. The results of the nutritional aspects that showed effectiveness in improving the progression of MS, are zinc, vitamin D, fiber, probiotics, fish oil and olive oil, cocoa, turmeric and salmon. There is evidence of the immunomodulatory role of Zn and vitamin D in inhibiting the production of proinflammatory citokines. Low levels of both components are associated with an increased risk of MS. Other components of nutritional interest are fiber and probiotics; they produce short chain fatty acids, with anti-inflammatory properties. The first is known for its role in gastrointestinal motility and the second one for its cellular and molecular actions in inflammatory processes and the microbiome modulation, to name a few. The nutrition aspects mentioned above, can contribute to modulate inflammation and improve fatigue. Finally, this paper creates an important perspective to continue the investigation concerning the influence of diet in MS patients.

scholarly journals The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis

2019 ◽  
Vol 77 (7) ◽  
pp. 1289-1317 ◽  
Author(s):  
Charlotte G. H. M. de Jong ◽  
Hans-Joachim Gabius ◽  
Wia Baron
Keyword(s):  
Multiple Sclerosis ◽  
Treatment Modalities ◽  
Unknown Etiology ◽  
Biological Mechanisms ◽  
Immune Mediator ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
Novel Therapeutic Strategies ◽  
Disease Modifying Treatment

Abstract Multiple sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease of the central nervous system with unknown etiology. Currently approved disease-modifying treatment modalities are immunomodulatory or immunosuppressive. While the applied drugs reduce the frequency and severity of the attacks, their efficacy to regenerate myelin membranes and to halt disease progression is limited. To achieve such therapeutic aims, understanding biological mechanisms of remyelination and identifying factors that interfere with remyelination in MS can give respective directions. Such a perspective is given by the emerging functional profile of galectins. They form a family of tissue lectins, which are potent effectors in processes as diverse as adhesion, apoptosis, immune mediator release or migration. This review focuses on endogenous and exogenous roles of galectins in glial cells such as oligodendrocytes, astrocytes and microglia in the context of de- and (re)myelination and its dysregulation in MS. Evidence is arising for a cooperation among family members so that timed expression and/or secretion of galectins-1, -3 and -4 result in modifying developmental myelination, (neuro)inflammatory processes, de- and remyelination. Dissecting the mechanisms that underlie the distinct activities of galectins and identifying galectins as target or tool to modulate remyelination have the potential to contribute to the development of novel therapeutic strategies for MS.

scholarly journals Neuroinflammation: A Potential Risk for Dementia

2022 ◽  
Vol 23 (2) ◽  
pp. 616
Author(s):  
Md Afroz Ahmad ◽  
Ozaifa Kareem ◽  
Mohammad Khushtar ◽  
Md Akbar ◽  
Md Rafiul Haque ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Cell Activation ◽  
Microglial Cell ◽  
Oxygen Species ◽  
Independent Function ◽  
Published Evidence ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
The Brain

Dementia is a neurodegenerative condition that is considered a major factor contributing to cognitive decline that reduces independent function. Pathophysiological pathways are not well defined for neurodegenerative diseases such as dementia; however, published evidence has shown the role of numerous inflammatory processes in the brain contributing toward their pathology. Microglia of the central nervous system (CNS) are the principal components of the brain’s immune defence system and can detect harmful or external pathogens. When stimulated, the cells trigger neuroinflammatory responses by releasing proinflammatory chemokines, cytokines, reactive oxygen species, and nitrogen species in order to preserve the cell’s microenvironment. These proinflammatory markers include cytokines such as IL-1, IL-6, and TNFα chemokines such as CCR3 and CCL2 and CCR5. Microglial cells may produce a prolonged inflammatory response that, in some circumstances, is indicated in the promotion of neurodegenerative diseases. The present review is focused on the involvement of microglial cell activation throughout neurodegenerative conditions and the link between neuroinflammatory processes and dementia.

scholarly journals Metal Imbalance in Neurodegenerative Diseases with a Specific Concern to the Brain of Multiple Sclerosis Patients

2020 ◽  
Vol 21 (23) ◽  
pp. 9105
Author(s):  
Jean-Philippe Dales ◽  
Sophie Desplat-Jégo
Keyword(s):  
Multiple Sclerosis ◽  
Neurodegenerative Diseases ◽  
Drug Targets ◽  
Chronic Inflammatory Disease ◽  
Autoimmune Reaction ◽  
Candidate Drug ◽  
The Central Nervous System ◽  
Multiple Sclerosis Patients ◽  
The Brain

There is increasing evidence that deregulation of metals contributes to a vast range of neurodegenerative diseases including multiple sclerosis (MS). MS is a chronic inflammatory disease of the central nervous system (CNS) manifesting disability and neurological symptoms. The precise origin of MS is unknown, but the disease is characterized by focal inflammatory lesions in the CNS associated with an autoimmune reaction against myelin. The treatment of this disease has mainly been based on the prescription of immunosuppressive and immune-modulating agents. However, the rate of progressive disability and early mortality is still worrisome. Metals may represent new diagnostic and predictive markers of severity and disability as well as innovative candidate drug targets for future therapies. In this review, we describe the recent advances in our understanding on the role of metals in brain disorders of neurodegenerative diseases and MS patients.

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