In the neurodegenerative phase of the disease, excessive amounts of glutamate are released by lymphocytes, microglia, and macrophages.27 The glutamate activates various glutamate receptors (AMPA and kainate receptors), and the influx of calcium through ion channels associated with different glutamate receptors may cause necrotic damage to oligodendrocytes and axons.
Memantine, a clinically employed drug with N-methyl-D-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rat experimental autoimmune encephalomyelitis (EAE). Interestingly, this therapeutic effect was not due to dampened CNS inflammation….
We have provided further strong evidence in support of a role for the NMDA receptor in the development of EAE and, in particular, the loss of BBB function and recruitment of inflammatory cells. Moreover, memantine is therapeutically efficacious, suggesting the NMDA receptor as a viable pharmacological target for future treatment of human neurological conditions such as multiple sclerosis.
All 11 patients with fixational pendular nystagmus who were given memantine, a glutamate antagonist, experienced complete cessation of the nystagmus.
Shayk wrote:Hope this gives you some “insight” about Namenda (memantine.) I haven’t actually read enough about its side effects to know if it might be the cause of the problems you’re experiencing though. Sorry.
Sharon (excited about the possibilities of memantine and can you believe it's not a hormone )
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