scholarly journals Five Decades of Cuprizone, an Updated Model to Replicate Demyelinating Diseases

2019 ◽  
Vol 17 (2) ◽  
pp. 129-141 ◽  
Author(s):  
Jose M. Vega-Riquer ◽  
Gerardo Mendez-Victoriano ◽  
Raul A. Morales-Luckie ◽  
Oscar Gonzalez-Perez
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Signs ◽  
Behavioral Changes ◽  
Demyelinating Diseases ◽  
Histological Changes ◽  
Cerebellar Peduncles ◽  
The Central Nervous System ◽  
Myelin Disorders ◽  
The Brain ◽  
Pharmacological Model

Introduction: Demyelinating diseases of the central nervous system (CNS) comprise a group of neurological disorders characterized by progressive (and eventually irreversible) loss of oligodendrocytes and myelin sheaths in the white matter tracts. Some of myelin disorders include: Multiple sclerosis, Guillain-Barré syndrome, peripheral nerve polyneuropathy and others. To date, the etiology of these disorders is not well known and no effective treatments are currently available against them. Therefore, further research is needed to gain a better understand and treat these patients. To accomplish this goal, it is necessary to have appropriate animal models that closely resemble the pathophysiology and clinical signs of these diseases. Herein, we describe the model of toxic demyelination induced by cuprizone (CPZ), a copper chelator that reduces the cytochrome and monoamine oxidase activity into the brain, produces mitochondrial stress and triggers the local immune response. These biochemical and cellular responses ultimately result in selective loss of oligodendrocytes and microglia accumulation, which conveys to extensive areas of demyelination and gliosis in corpus callosum, superior cerebellar peduncles and cerebral cortex. Remarkably, some aspects of the histological pattern induced by CPZ are similar to those found in multiple sclerosis. CPZ exposure provokes behavioral changes, impairs motor skills and affects mood as that observed in several demyelinating diseases. Upon CPZ removal, the pathological and histological changes gradually revert. Therefore, some authors have postulated that the CPZ model allows to partially mimic the disease relapses observed in some demyelinating diseases. Conclusion: for five decades, the model of CPZ-induced demyelination is a good experimental approach to study demyelinating diseases that has maintained its validity, and is a suitable pharmacological model for reproducing some key features of demyelinating diseases, including multiple sclerosis.

scholarly journals Is that a scolex? a case of clinically isolated syndrome

2019 ◽  
Vol 6 (6) ◽  
pp. 2697
Author(s):  
Van K. Ma ◽  
Lourdemillard Bellevue ◽  
Maria Espiritu Fuller
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Clinically Isolated Syndrome ◽  
Mri Brain ◽  
Demyelinating Lesions ◽  
The Central Nervous System ◽  
Clinical Signs And Symptoms ◽  
The Brain

Clinically Isolated Syndrome is an initial demyelinating event of the central nervous system that has been associated with the future development of multiple sclerosis. Diagnostic studies include clinical and paraclinical studies. Patients with lesions on MRI of the brain at baseline will more likely develop multiple sclerosis compared to patients without findings. We report a case of a 10-year-old female of Colombian ancestry and origin, who presented with indiscernible neurological clinical signs and symptoms, with MRI brain with and without contrast showing demyelinating lesions with one lesion “suggesting” a scolex.

Depression and Inflammatory Markers in Veterans With Multiple Sclerosis

2021 ◽  
pp. 109980042110500
Author(s):  
Pamela Newland ◽  
Yelyzaveta Basan ◽  
Ling Chen ◽  
Gregory Wu
Keyword(s):  
Multiple Sclerosis ◽  
Inflammatory Markers ◽  
Pearson Correlation ◽  
Correlation Coefficients ◽  
The United States ◽  
Biological Mechanisms ◽  
The Central Nervous System ◽  
Brain And Spinal Cord ◽  
The Brain

Multiple sclerosis (MS), an inflammatory neurodegenerative disease of the central nervous system (CNS), afflicts over one per thousand people in the United States. The pathology of MS typically involves lesions in several regions, including the brain and spinal cord. The manifestation of MS is variable and carries great potential to negatively impact quality of life (QOL). Evidence that inflammatory markers are related to depression in MS is accumulating. However, there are barriers in precisely identifying the biological mechanisms underlying depression and inflammation. Analysis of cytokines provides one promising approach for understanding the mechanisms that may contribute to MS symptoms. Methods: In this pilot study, we measured salivary levels of interleukin (IL)-6, IL-1beta (β), and IL-10 in 24 veterans with MS. Descriptive statistics were reported and Pearson correlation coefficients were obtained between cytokines and depression. Results: The anti-inflammatory cytokine IL-10 was significantly negatively associated with depression in veterans with MS (r = −0.47, p = .024). Conclusion: Cytokines may be useful for elucidating biological mechanisms associated with the depression and a measure for nurses caring for veterans with MS.

scholarly journals Metabolomic Signature in Sera of Multiple Sclerosis Patients during Pregnancy

2018 ◽  
Vol 19 (11) ◽  
pp. 3589 ◽  
Author(s):  
Claudia Rossi ◽  
Ilaria Cicalini ◽  
Mirco Zucchelli ◽  
Maria di Ioia ◽  
Marco Onofrj ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Signs ◽  
Female Gender ◽  
Epidemiological Studies ◽  
Mass Spectrometry Analysis ◽  
Spectrometry Analysis ◽  
Hormonal Fluctuations ◽  
The Central Nervous System ◽  
Multiple Sclerosis Patients

Multiple sclerosis (MuS) is an autoimmune disease of the central nervous system characterized by neuroinflammation, neurodegeneration, and degradation of the myelin sheath. Epidemiological studies have shown that the female gender is more susceptible than the male gender to MuS development, with a female-to-male ratio of 2:1. Despite this high onset, women have a better prognosis than men, and the frequency of the relapsing phase decreases during pregnancy, while it increases soon after birth. Therefore, it is interesting to investigate hormonal fluctuations during pregnancy and whether they correlate with metabolic signatures. To gain a deeper inside into the biochemical mechanism of such a multifactorial disease, we adopted targeted metabolomics approaches for the determination of many serum metabolites in 12 pregnant women affected by MuS by mass spectrometry analysis. Our data show a characteristic hormonal fluctuation for estrogens and progesterone, as expected. They also highlight other interesting hormonal alterations for cortisol, corticosterone, 11-deoxycortisol, 4-androstene-3,17-dione, testosterone, and 17α-hydroxyprogesterone. Furthermore, a negative correlation with progesterone levels was observed for amino acids and for acylcarnitines, while an imbalance of different sphingolipids pathways was found during pregnancy. In conclusion, these data are in agreement with the characteristic clinical signs of MuS patients during pregnancy and, if confirmed, they may add an important tessera in the complex mosaic of maternal neuroprotection.

scholarly journals PECULIARITIES OF THE CLINICAL COURSE OF POSTMEASLES ENCEPHALITIS IN IMMUNOSUPRESSED PEOPLE

2021 ◽  
Vol 64 (1) ◽  
Author(s):  
Tetiana Nehrych ◽  
◽  
Maria Shorobura ◽  
Irina Hritsyna ◽  
Liliia Yukhimiv ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Monoclonal Antibodies ◽  
Inclusion Body ◽  
Bacterial Pneumonia ◽  
Clinical Course ◽  
Risk Group ◽  
Neurological Complications ◽  
Immunosuppressive Drugs ◽  
The Central Nervous System ◽  
The Brain

Primary acute measles encephalitis and acute postmeasles encephalitis are the most common neurological complications of measles. It is important to detect encephalitis, which develops a month or more after the manifestations of measles infection. These encephalitis are rare and occur mainly in people with immunodefi ciency. Multiple sclerosis is a chronic disease of the central nervous system for the treatment of which diseasemodifying therapy is used, namely monoclonal antibodies, that can lead to immunosuppression and immunodefi ciency. Nowadays, there is insuffi cient information about the course of postcortical encephalitis in patients with multiple sclerosis who are taking immunosuppressive drugs. The article presents data on the clinical classifi cation, diagnosis and treatment of measles encephalitis. A clinical case of measles inclusion body encephalitis in a thirty-threeyear-old patient with multiple sclerosis on the background of annual intake of monoclonal antibodies is presented. She also had viral-bacterial pneumonia and developed disseminated intravascular coagulation in the brain and lungs. These complications of measles infection led to the death of the person after a month and a half of intensive care. Thus, patients with multiple sclerosis who are taking drugs with immunosuppressive eff ects are among the risk group for measles inclusion body encephalitis. Measles inclusion body encephalitis in such patients can be severe, which complicates timely diagnosis, proper treatment and leads to death.

scholarly journals Ozone therapy in ethidium bromide-induced demyelination in rats: possible protective effect [abstract]

2019 ◽  
Vol 3 (4) ◽  
Author(s):  
Mohga Samy
Keyword(s):  
Multiple Sclerosis ◽  
Protective Effect ◽  
Ethidium Bromide ◽  
Demyelinating Diseases ◽  
Immune Reactivity ◽  
Methyl Prednisolone ◽  
The Central Nervous System ◽  
Group 5 ◽  
Group 2 ◽  
Oxygen Groups

BACKGROUND: Multiple sclerosis is an autoimmune inflammatory disease of the central nervous system and it is characterized by excessive demyelination PURPOSE: The study aim to investigate the possible protective effect of ozone (O3) in ethidium bromide (EB) induced demyelination in rats either alone or in combination with corticosteroid in order to decreases the dose of steroid therapy. MATERIAL and METHODS: Rats were divided into 7 groups Group (1) normal control rats received saline. Group (2) sham-operated rats received saline. Group (3) sham operated rats received oxygen. Group (4) EB-treated rats received EB. Group (5) EB treated rats received oxygen. Group (6) EB treated rats received methyl prednisolone (MP) Group (7) EB treated rats received half the dose of MP concomitant with ozone. RESULTS: Significant improvement in the brain serotonin, dopamine, noradrenalin. A reduction of MDA,TNF-COX2 immune-reactivity was noticed in MP and oxygen groups . Furthermore, best amelioration was achieved by combining half the dose of methyl-prednisolone with ozone. CONCLUSION: We concluded that ozone has a protective effect on demyelination and can be used due to its protective effect in demyelinating diseases such as multiple sclerosis.

Demyelinating disorders of the central nervous system

2010 ◽  
pp. 4948-4963
Author(s):  
Siddharthan Chandran ◽  
Alastair Compston
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Acute Disseminated Encephalomyelitis ◽  
Demyelinating Diseases ◽  
Demyelinating Disorder ◽  
System P ◽  
The Central Nervous System ◽  
Demyelinating Disorders ◽  
Brain And Spinal Cord

Clinicians suspect demyelination when episodes reflecting damage to white matter tracts within the central nervous system occur in young adults. The paucity of specific biological markers of discrete demyelinating syndromes places an emphasis on clinical phenotype—temporal and spatial patterns—when classifying demyelinating disorders. The diagnosis of multiple sclerosis, the most common demyelinating disorder, becomes probable when these symptoms and signs recur, involving different parts of the brain and spinal cord. Other important demyelinating diseases include post-infectious neurological disorders (acute disseminated encephalomyelitis), demyelination resulting from metabolic derangements (central pontine myelinosis), and inherited leucodystrophies that may present in children or in adults. Accepting differences in mechanism, presentation, and treatment, two observations can usefully be made when classifying demyelinating disorders. These are the presence or absence of inflammation, and the extent of focal vs. diffuse demyelination. Multiple sclerosis is prototypic for the former, whereas dysmyelinating disorders, such as leucodystrophies are representative of the latter....

scholarly journals Presence of amastigotes in the central nervous system of hamsters infected with Leishmania sp.

2011 ◽  
Vol 20 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Elisangela de Oliveira ◽  
Elisa Teruya Oshiro ◽  
Rebeca Vieira Pinto ◽  
Bruna Corrêa de Castro ◽  
Karla Borges Daniel ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Signs ◽  
Direct Examination ◽  
Mato Grosso ◽  
The Central Nervous System ◽  
Animal House ◽  
Immunohistochemical Studies ◽  
Negative Controls ◽  
The Brain

Visceral leishmaniasis (VL) is a severe chronic disease caused by Leishmania (Leishmania) infantum chagasi. Better knowledge on the effects caused by this disease can help develop adequate clinical management and treatment. Parasitological and immunohistochemical studies were performed golden hamsters Mesocricetus auratus infected with bone marrow from individuals with VL in the State of Mato Grosso do Sul, central-west Brazil. The effects of parasitism in the spleen, liver, kidneys, lungs, heart and brain of the animals were examined. Eighteen hamsters were inoculated intraperitoneally, and six healthy animals were used as negative controls. The animals were kept in the animal house and checked for clinical signs. Specimens of each organ were examined for the presence of amastigotes. Immunohistochemical technique was performed in all brain specimens and organs negative on the direct examination of parasites. Direct examination of amastigotes was positive in the spleen and liver of all infected animals; 33.3% showed the parasite in the kidneys and lungs, and 16.7% in the heart. Parasitic forms were seen in 83.3% (15/18) of the brain examined. Immunohistochemistry confirmed the results of the direct examination, except in two specimens of lung tissue and in the brain specimens. Other studies are needed to further clarify the effect of the parasite in the central nervous system.

scholarly journals Differential diagnosis of suspected multiple sclerosis: a consensus approach

2008 ◽  
Vol 14 (9) ◽  
pp. 1157-1174 ◽  
Author(s):  
DH Miller ◽  
BG Weinshenker ◽  
M Filippi ◽  
BL Banwell ◽  
JA Cohen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Differential Diagnosis ◽  
Evidence Base ◽  
Demyelinating Diseases ◽  
Future Research ◽  
International Panel ◽  
The Central Nervous System ◽  
Definition Of ◽  
Demyelinating Disorders ◽  
Diagnosis Criteria

Background and objectives Diagnosis of multiple sclerosis (MS) requires exclusion of diseases that could better explain the clinical and paraclinical findings. A systematic process for exclusion of alternative diagnoses has not been defined. An International Panel of MS experts developed consensus perspectives on MS differential diagnosis. Methods Using available literature and consensus, we developed guidelines for MS differential diagnosis, focusing on exclusion of potential MS mimics, diagnosis of common initial isolated clinical syndromes, and differentiating between MS and non-MS idiopathic inflammatory demyelinating diseases. Results We present recommendations for 1) clinical and paraclinical red flags suggesting alternative diagnoses to MS; 2) more precise definition of “clinically isolated syndromes” (CIS), often the first presentations of MS or its alternatives; 3) algorithms for diagnosis of three common CISs related to MS in the optic nerves, brainstem, and spinal cord; and 4) a classification scheme and diagnosis criteria for idiopathic inflammatory demyelinating disorders of the central nervous system. Conclusions Differential diagnosis leading to MS or alternatives is complex and a strong evidence base is lacking. Consensus-determined guidelines provide a practical path for diagnosis and will be useful for the non-MS specialist neurologist. Recommendations are made for future research to validate and support these guidelines. Guidance on the differential diagnosis process when MS is under consideration will enhance diagnostic accuracy and precision.

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.

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