myelitis/tyrosine

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Inhibition of tyrosine kinase-mediated cellular signalling by Tyrphostins AG126 and AG556 modulates secondary damage in experimental spinal cord trauma.

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Protein tyrosine kinases help to regulate the expression of many genes, which play an important role in the pathophysiology of a number of diseases. Here we investigate the effects of the tyrosine kinase inhibitors, AG126 and AG556 on the degree of experimental spinal cord trauma induced by the

CNS demyelination after initiating the tyrosine kinase inhibitor imatinib: A report of two cases.

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The tyrosine kinase inhibitor, imatinib, used to treat certain malignancies, is in clinical trials as a potential treatment for multiple sclerosis and acute stroke. This is the first report of cases of multifocal central nervous system (CNS) demyelination following exposure to imatinib. One case was

Glatiramer acetate could be a hypothetical therapeutic agent for neuromyelitis optica.

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Neuromyelitis optica (NMO) is characterized by concurrence of optic neuritis and transverse myelitis, which is typically associated with a spinal cord lesion extending three or more vertebral segments. NMO is an inflammatory, demyelinating central nervous system disorder, and although it has a

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