IgG stimulated remyelination of peripheral nerves
US-10494418-B2 · Dec 3, 2019 · US
US9834593B2 · US · B2
| Field | Value |
|---|---|
| Publication number | US-9834593-B2 |
| Application number | US-201514625542-A |
| Country | US |
| Kind code | B2 |
| Filing date | Feb 18, 2015 |
| Priority date | Feb 29, 2012 |
| Publication date | Dec 5, 2017 |
| Grant date | Dec 5, 2017 |
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The present invention is based on the discovery of polyclonal IgG's ability to promote Schwann cell maturation, differentiation, and myelin production. Methods for treating non-idiopathic, demyelinating peripheral neuropathies in mammals, where the neuropathy is not immune-mediated or infection-mediated, through the administration of polyclonal IgG are provided. Types of demyelinating peripheral neuropathies treatable with the present invention include peripheral nerve trauma and toxin-induced peripheral neuropathies. Alternatively, a composition of polyclonal IgGs can be applied directly to a peripheral nerve cell to induce maturation, differentiation into a myelinating state, and myelin expression or promote cell survival.
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What is claimed is: 1. A method of treating a demyelinating peripheral neuropathy comprising administering a therapeutically effective amount of polyclonal IgG to a mammal diagnosed with said neuropathy, wherein said demyelinating neuropathy is a toxin-induced neuropathy, wherein the polyclonal IgG is administered intravenously, parenterally, or intra-arterially to the site affected by the toxin. 2. The method of claim 1 , wherein the mammal is human. 3. The method of claim 1 , wherein an anti-inflammatory agent is co-administered with the polyclonal IgG to the mammal. 4. The method of claim 3 , wherein the anti-inflammatory agent is adrenocorticotropic hormone, a corticosteroid, an interferon, glatiramer acetate, or a non-steroidal anti-inflammatory drug. 5. The method of claim 1 , wherein the toxin-induced neuropathy is induced by drugs and medications, industrial chemicals, or environmental toxins. 6. The method of claim 5 , wherein the toxin-induced neuropathy is induced by drugs and medications. 7. The method of claim 5 , wherein the toxin-induced neuropathy is induced by industrial chemicals. 8. The method of claim 5 , wherein the toxin-induced neuropathy is induced by environmental. 9. The method of claim 1 , wherein the polyclonal IgG is administered weekly. 10. The method of claim 1 , wherein the polyclonal IgG is administered biweekly. 11. The method of claim 1 , wherein the polyclonal IgG is administered monthly. 12. The method of claim 1 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.05 to 5 g per kg of patient body weight. 13. The method of claim 12 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.5 to 2 g per kg of patient body weight. 14. The method of claim 1 , wherein said toxin-induced neuropathy is not infection-mediated. 15. A method of treating a demyelinating peripheral neuropathy comprising administering a therapeutically effective amount of polyclonal IgG to a mammal diagnosed with said neuropathy, wherein said demyelinating neuropathy is an inherited neuropathy and excludes Guillain-Barré syndrome, chronic demyelinating polyneuropathy and multifocal motor neuropathy, wherein the polyclonal IgG is administered intravenously, parenterally, or intra-arterially to the site affected by the inherited neuropathy. 16. The method of claim 15 , wherein the mammal is human. 17. The method of claim 15 , wherein an anti-inflammatory agent is co-administered with the polyclonal IgG to the mammal. 18. The method of claim 17 , wherein the anti-inflammatory agent is adrenocorticotropic hormone, a corticosteroid, an interferon, glatiramer acetate, or a non-steroidal anti-inflammatory drug. 19. The method of claim 15 , wherein the inherited neuropathy is selected from the group consisting of Charcot-Marie-Tooth disease, Abetalipoproteinemia, Tangier disease, Metachromatic leukodystrophy, Fabry's disease, and Dejerine-Sottas syndrome. 20. The method of claim 19 , wherein the inherited neuropathy is Charcot-Marie-Tooth disease. 21. The method of claim 19 , wherein the inherited neuropathy is Abetalipoproteinemia. 22. The method of claim 19 , wherein the inherited neuropathy is Tangier disease. 23. The method of claim 19 , wherein the inherited neuropathy is Metachromatic leukodystrophy. 24. The method of claim 19 , wherein the inherited neuropathy is Fabry's disease. 25. The method of claim 19 , wherein the inherited neuropathy is Dejerine-Sottas syndrome. 26. The method of claim 15 , wherein the demyelinating peripheral neuropathy is motor neuropathy. 27. The method of claim 15 , wherein the demyelinating peripheral neuropathy is sensory neuropathy. 28. The method of claim 15 , wherein the demyelinating peripheral neuropathy is sensorimotor neuropathy. 29. The method of claim 15 , wherein the demyelinating peripheral neuropathy is autonomic neuron neuropathy. 30. The method of claim 15 , wherein the polyclonal IgG is administered weekly. 31. The method of claim 15 , wherein the polyclonal IgG is administered biweekly. 32. The method of claim 15 , wherein the polyclonal IgG is administered monthly. 33. The method of claim 15 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.05 to 5 g per kg of patient body weight. 34. The method of claim 33 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.5 to 2 g per kg of patient body weight. 35. The method of claim 15 , wherein said inherited neuropathy is not infection-mediated.
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