Multiple Sclerosis

Brass, Steven D.; Weiner, Howard L.; Hafler, David A.

doi:10.1016/b978-012595961-2/50049-4

Cited by 3 publications

(5 citation statements)

References 144 publications

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“…Tiredness, depression and cognitive impairment are also considered as common symptoms. 1,11 The typical signs of MS, moreover, are the clinical symptoms and the varied course of the disease. Multiple sclerosis can be divided into four clinical categories, namely Clinically Isolated Syndrome (CIS), Relapsing Remitting Multiple Sclerosis (RRMS), Secondary Progressive Multiple Sclerosis (SPMS) and Primary Progressive Multiple Sclerosis (PPMS).…”

Section: Pathogenesismentioning

confidence: 99%

“…SPMS patients are those who do not have the onset of acute attacks, but from the beginning there is a gradual clinical deterioration. 1,12…”

Section: Pathogenesismentioning

confidence: 99%

“…When electrophoresis examination is performed on the normal cerebrospinal fluid (CSS), it will generate results in a homogeneous blur of immunoglobulin, whereas in MS patients there will be some lines showing excessive antibody production (Figure 2). 1,16,19…”

Section: Oligoclonal Immunoglobulin Bands (Ocbs)mentioning

confidence: 99%

“…Charcot then revealed accumulation of inflammatory cells in the perivascular and demyelinating areas together with plaques found in the substrate of brain alba and spinal cord in patients with intermittent neurological deficits, resulting in the term "sclérose en plaques disseminées" or multiple sclerosis. 1 Multiple sclerosis is an autoimmune disease that causes myelin destruction in the Central Nervous System (CNS). Characteristics of this disease are perivascular infiltration by inflammatory cells, demyelination and loss of axons, accompanied by mul-multiple plaque formation in the brain and spinal cord.…”

Section: Introductionmentioning

confidence: 99%

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Immunology of Multiple Sclerosis

Bahrun

Wijaya

2018

Indonesian J. Clin. Pathol. Med. Lab.

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Multiple Sclerosis (MS) is an autoimmune disease that causes myelin destruction in the Central Nervous System (CNS). Characteristics of this disease are perivascular infiltration by inflammatory cells, demyelination and loss of axons, accompanied by multiple plaque formation in the brain and spinal cord. According to the National Multiple Sclerosis Society, 400,000 people suffer from MS in the United States and about 2.5 million people worldwide. The disease is usually diagnosed in patients aged 20-45 years and more often found in females than males with a ratio of 2: 1. Nevertheless, the etiology of MS is still unknown, but it is suspected that genetic and environmental factors may induce a response to central nervous system autoantigen, such as Epstein-Barr Virus (EBV) infection. It then causes edema, demyelination, axon destruction and loss of oligodendrosites, resulting in neurological deficits, plaque formation, scarring and reduced brain volume. Multiple sclerosis symptoms and signs actually vary greatly depending on the location of the lesions and the course of the various diseases. Multiple sclerosis, moreover, can be divided into four clinical categories, namely Clinically Isolated Syndrome (CIS), Relapsing Remitting Multiple Sclerosis (RRMS), Secondary Progressive Multiple Sclerosis (SPMS) and Primary Progressive Multiple Sclerosis (PPMS). Diagnosis of Multiple sclerosis is established based on clinical symptoms and supporting investigations, such as MRI, CSF and neurological examination. In CSF examination, oligoclonal bands are found in over 90% of patients, considered as one of the laboratory criteria supporting the diagnosis of MS. There are four kinds of drugs that have been approved by the FDA as disease modifying therapy for the initial treatment of MS patients, namely interferon beta-1a, subcutaneous (SC) interferon beta-1a, interferon beta-1b and glatiramer acetate In conclusion, life expectancy in MS patients is only slightly reduced and survival is related to the disability occurred.

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Section: Pathogenesismentioning

confidence: 99%

“…SPMS patients are those who do not have the onset of acute attacks, but from the beginning there is a gradual clinical deterioration. 1,12…”

Section: Pathogenesismentioning

confidence: 99%

Section: Oligoclonal Immunoglobulin Bands (Ocbs)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Immunology of Multiple Sclerosis

Bahrun

Wijaya

2018

Indonesian J. Clin. Pathol. Med. Lab.

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“…Cyclophosphamide is an oxazaphosphorine, alkylating agent of the nitrogen mustard class with potent cytotoxic and immunosuppressive effects; first synthesized by Arnold and colleagues in 1958 [ 1 – 3 ]. It is widely used in the treatment of malignant tumors and autoimmune diseases including lupus, systemic sclerosis, and several types of vasculitides [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Potential Protective Effects of Antioxidants against Cyclophosphamide-Induced Nephrotoxicity

Ayza

Zewdie

Yigzaw

et al. 2022

International Journal of Nephrology

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Cyclophosphamide is an alkylating antineoplastic agent, and it is one of the most successful drugs with wide arrays of clinical activity. It has been in use for several types of cancer treatments and as an immunosuppressive agent for the management of autoimmune and immune-mediated diseases. Nowadays, its clinical use is limited due to various toxicities, including nephrotoxicity. Even though the mechanisms are not well understood, cyclophosphamide-induced nephrotoxicity is reported to be mediated through oxidative stress. This review focuses on the potential role of natural and plant-derived antioxidants in preventing cyclophosphamide-induced nephrotoxicity.

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Methylprednisolone induces reversible clinical and pathological remission and loss of lymphocyte reactivity to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis

et al. 2008

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Experimental autoimmune encephalomyelitis (EAE) is an animal model of human multiple sclerosis (MS). EAE, induced by immunisation with myelin-associated autoantigens, is characterised by an inflammatory infiltrate in the central nervous system (CNS) associated with axonal degeneration, demyelination and damage. We have recently shown in an experimental mouse model of autoimmune gastritis that methylprednisolone treatment induces a reversible remission of gastritis with regeneration of the gastric mucosa. Here, we examined the effect of oral methylprednisolone on the mouse EAE model of human MS induced by immunisation with myelin oligodendrocyte glycoprotein peptide (MOG(35-55)). We examined the clinical scores, CNS pathology and lymphocyte reactivity to MOG(35-55) following treatment and withdrawal of the steroid. Methylprednisolone remitted the clinical signs of EAE and the inflammatory infiltrate in the CNS, accompanied by loss of lymphocyte reactivity to MOG(35-55) peptide. Methylprednisolone withdrawal initiated relapse of the clinical features, a return of the CNS inflammatory infiltrate and lymphocyte reactivity to MOG(35-55) peptide. This is the first study to show that methylprednisolone induced a reversible remission in the clinical and pathological features of EAE in mice accompanied by loss of lymphocyte reactivity to the encephalitogen. This model will be useful for studies directed at a better understanding of mechanisms associated with steroid-induced disease remission, relapse and remyelination and also as an essential adjunct to an overall curative strategy.

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Multiple Sclerosis

Cited by 3 publications

References 144 publications

Immunology of Multiple Sclerosis

Immunology of Multiple Sclerosis

Potential Protective Effects of Antioxidants against Cyclophosphamide-Induced Nephrotoxicity

Methylprednisolone induces reversible clinical and pathological remission and loss of lymphocyte reactivity to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis

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