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)

1. Brain homogenates of mice infected with the Theiler FA strain of mouse encephalomyelitis virus show marked inhibition of glucose phosphorylation. 2. A similar effect can be obtained by incubating normal brain homogenates with small amounts of ferrous sulfate. 3. Partially purified preparations of Theiler FA virus contain iron in amounts corresponding to their inhibitory effect on brain glycolysis. The virus preparations were purified by chemical fractionation and differential centrifugation and were dialyzed against potassium cyanide or pyrophosphate and potassium chloride for several days before they were analyzed for iron content. 4. The inhibitory effect of the virus preparations and of ferrous sulfate has been shown to be dependent on a heat-labile factor present in normal brain ("inactivating factor"). 5. The glycolytic activity of brain homogenates of mice infected with the Theiler FA virus can be restored by addition of a factor prepared from rabbit muscle extract. This "restoring factor" is non-dialyzable and is heat-labile. It has no hexokinase or phosphohexokinase activity. Its restoring activity is destroyed by the "inactivating factor" present in brain.
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PMID:RELATION OF IRON SALTS TO INHIBITION OF GLYCOLYSIS BY THEILER FA VIRUS OF MOUSE ENCEPHALOMYELITIS. 1987 45

Neuroinflammation can cause major neurological dysfunction, without demyelination, in both multiple sclerosis (MS) and a mouse model of the disease (experimental autoimmune encephalomyelitis; EAE), but the mechanisms remain obscure. Confocal in vivo imaging of the mouse EAE spinal cord reveals that impaired neurological function correlates with the depolarisation of both the axonal mitochondria and the axons themselves. Indeed, the depolarisation parallels the expression of neurological deficit at the onset of disease, and during relapse, improving during remission in conjunction with the deficit. Mitochondrial dysfunction, fragmentation and impaired trafficking were most severe in regions of extravasated perivascular inflammatory cells. The dysfunction at disease onset was accompanied by increased expression of the rate-limiting glycolytic enzyme phosphofructokinase-2 in activated astrocytes, and by selective reduction in spinal mitochondrial complex I activity. The metabolic changes preceded any demyelination or axonal degeneration. We conclude that mitochondrial dysfunction is a major cause of reversible neurological deficits in neuroinflammatory disease, such as MS.
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PMID:Mitochondrial dysfunction is an important cause of neurological deficits in an inflammatory model of multiple sclerosis. 2762 21