Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myelin-oligodendrocyte glycoprotein (MOG) has been implicated as a target for antibody-mediated immune attack in experimental autoimmune encephalomyelitis (EAE) which has been used extensively as an experimental model of multiple sclerosis (MS). We have screened cerebrospinal fluid (CSF) and plasma from 30 patients with MS, 30 with other neurological diseases (OND) and 30 with tension headache for anti-MOG antibodies of IgG isotype by enzyme-linked immunosorbent assay (ELISA). Such antibodies were detected in CSF from seven of the patients with MS, compared to two with OND and one with tension headache. No anti-MOG IgG antibodies were demonstrable in plasma. Antibody specificity was confirmed by Western blot immunostaining. Antibody levels were higher in MS compared to OND and tension headache. No correlation was observed between anti-MOG IgG antibodies and total IgG levels in CSF. The significance of anti-MOG antibodies demonstrated in MS CSF remains to be defined.
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PMID:Antibodies to myelin-oligodendrocyte glycoprotein in cerebrospinal fluid from patients with multiple sclerosis and controls. 199 22

Nitric oxide (NO) may be involved in myelin and oligodendrocyte injury associated with multiple sclerosis (MS), a demyelinating disease of unknown etiology. The cerebrospinal fluid (CSF) from MS patients may provide an important signal inducing a pathologic process within the central nervous system (CNS). To investigate this question, CSF-induced NO production by glial cells was studied in 38 patients with multiple sclerosis (MS), 30 patients with other CNS inflammatory diseases (ID) and 20 with tension headache (TH) as control. Neuron damage was estimated by release of lactate dehydrogenase (LDH), whereas oligodendrocyte damage was estimated by a percentage of viable cells in primary oligodendrocyte cultures. Here we show that CSFs from 13/38 (34%) patients with MS stimulate glial cells to produce NO, compared to 2/20 (10%) of patients with ID and 1/30 (3%) with tension headache. The levels of NO production correlated positively with the amounts of LDH released and negatively with percentage of viable oligodendrocytes, suggesting that NO may represent a mechanism for oligodendrocyte losses in affected tissues and play a role in lesion formation in MS and its animal model experimental allergic encephalomyelitis (EAE).
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PMID:The cerebrospinal fluid from patients with multiple sclerosis promotes neuronal and oligodendrocyte damage by delayed production of nitric oxide in vitro. 890 30