multiple sclerosis/protease

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Prevention of acute autoimmune encephalomyelitis and abrogation of relapses in murine models of multiple sclerosis by the protease inhibitor D-penicillamine.

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The in vitro activity of gelatinase B, an enzyme whose appearance in the cerebrospinal fluid is associated with inflammatory diseases of the central nervous system, was dose-dependently inhibited by the antirheumatic D-penicillamine. Inhibition of gelatinase B in electrophoretically pure

Influence of ACTH on activity of some granulocytic proteases in patients with multiple sclerosis.

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The effect of treatment with ACTH on activity of granulocytic acid and neutral proteases in patients suffering from multiple sclerosis was studied. Protease activity was distinctly higher in granulocytes from patients. ACTH normalized the activities investigated in patients with exacerbating course

Neutral protease in cerebrospinal fluid from patients with multiple sclerosis and other neurological diseases.

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Neutral protease activity was significantly elevated in the cerebro-spinal fluid of patients with multiple sclerosis (MS) in exacerbation and in the acute phase of acute viral meningoencephalitis (AME) compared with that of MS in remission, amyotrophic lateral sclerosis or psychosomatic disease.

[Changes in the protease inhibitor activity of the blood serum in patients with disseminated sclerosis].

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Changes in the blood serum protease inhibitors activity alpha 1-antitrypsin and antithrombin III were studied in 60 patients with multiple sclerosis. The activity of the inhibitors under study was found to be dependent upon the severity of the pathological process as well as on the age of the

[Diagnostic and pathogenetic implications of the site specificity of antibody proteases in multiple sclerosis].

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Disseminated sclerosis is currently regarded as a CNS autoimmune disease. One of the mechanisms behind this pathology is antibody (AB) formation. In this context, recent data on AB with proteolytic activity are of importance because they participate in selective proteolysis of myelin proteins in

Polymorphonuclear neutral protease activity in multiple sclerosis and other diseases.

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Polymorphonuclear neutral protease activity (PMN-NPA) was examined in 87 patients with definite multiple sclerosis (MS) (48 active, 39 inactive), 49 patients with other neurological diseases (OND), 24 patients with immune-mediated non-neurological diseases (INND), and 32 normal subjects. PMN-NPA was

Differential expression of protease M/neurosin in oligodendrocytes and their progenitors in an animal model of multiple sclerosis.

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To determine the possible involvement of protease M/neurosin in demyelinating diseases of the CNS, we examined its expression in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), a recognized animal model of multiple sclerosis (MS). In situ

Elevated neutral protease activity in myelin from brains of patients with multiple sclerosis.

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Incubation of human myelin at neutral pH resulted in the proteolytic conversion of the myelin-associated glycoprotein to a lower molecular weight derivative (dMAG) and the degradation of basic protein. The formation of dMAG occurred much more rapidly than the degradation of basic protein. The

The protease inhibitor, Bowman-Birk Inhibitor, suppresses experimental autoimmune encephalomyelitis: a potential oral therapy for multiple sclerosis.

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Available treatments for multiple sclerosis (MS) require frequent injections and have significant side effects. Proteases generated during inflammation are involved in the induction of tissue damage during inflammatory demyelination in the central nervous system (CNS). The Bowman-Birk Inhibitor

Latent-period stool proteomic assay of multiple sclerosis model indicates protective capacity of host-expressed protease inhibitors.

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Diseases are often diagnosed once overt symptoms arise, ignoring the prior latent period when effective prevention may be possible. Experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, exhibits such disease latency, but the molecular processes underlying this asymptomatic

Pharmacological inhibition of MALT1 protease activity protects mice in a mouse model of multiple sclerosis.

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BACKGROUND The paracaspase mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is crucial for lymphocyte activation through signaling to the transcription factor NF-κB. Besides functioning as a scaffold signaling protein, MALT1 also acts as a cysteine protease that

Assessment of protease-binding by alpha 2 macroglobulin in multiple sclerosis.

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Increased protease activity and changes in basic proteins and lipids in multiple sclerosis plaques.

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Toll-like receptor 4 and protease-activated receptor 2 in physiology and pathophysiology of the nervous system: more than just receptor cooperation?

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Toll-like receptor 4 (TLR4) and protease-activated receptor 2 (PAR2) play pivotal roles in the mammalian innate immune response. Notably, in addition to their involvement in detection of invading pathogens, PAR2 and TLR4 modulate the levels of cell death-induced sterile inflammation by activating

Degradation of basic protein in myelin by neutral proteases secreted by stimulated macrophages: a possible mechanism of inflammatory demyelination.

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In inflammatory demyelinating diseases such as multiple sclerosis and experimental allergic encephalomyelitis, myelin destruction occurs in the vicinity of infiltrating mononuclear cells. The observations that myelin can be altered prior to phagocytosis and in areas not contiguous with inflammatory

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