Glatiramer in the treatment of multiple sclerosis

International Journal of Nanomedicine

Volumn 1, Issue 3, 2006, Pages 283-289

  Rizvi, Syed A ^a   Kim, Edward ^a   Moodie, Jennifer ^a  

^a RHODE ISLAND HOSPITAL   (United States)

Author keywords

Clinical trials; Disease modifying agents; Glatiramer acetate; MRI; Multiple sclerosis; Neurodegeneration

Indexed keywords

GLATIRAMER; IMMUNOSUPPRESSIVE AGENT; NEUROPROTECTIVE AGENT; PEPTIDE;

BIOLOGICAL MODEL; CLINICAL TRIAL; HUMAN; IMMUNOLOGY; MULTIPLE SCLEROSIS; RECURRENT DISEASE; REVIEW;

CLINICAL TRIALS; HUMANS; IMMUNOSUPPRESSIVE AGENTS; MODELS, IMMUNOLOGICAL; MULTIPLE SCLEROSIS; NEUROPROTECTIVE AGENTS; PEPTIDES; RECURRENCE;

EID: 34548751720     PISSN: 11769114     EISSN: 11782013     Source Type: Journal    
DOI: None     Document Type: Review

References (53)

1. Abramsky O, Teitelbaum D, Arnon R. 1977. Effect of a synthetic polypeptide (Cop 1) on patients with multiple sclerosis and with acute disseminated encephalomyelitis. J Neurol Sci, 31:433-8.
2. Aharoni R, Kayhan B, Eilam R, et al. 2003. Glatiramer acetate-specific T cells in the brain express T helper 2/3 cytokines and brain-derived neurotrophic factor in situ. Proc Natl Acad Sci U S A, 100:14157-62.
3. Azoulay D, Vachapova V, Shihman B, et al. 2005. Lower brain-derived neurotrophic factor in serum of relapsing-remitting MS: Reversal by glatiramer acetate. J Neuroimmunol, 167: 215-18.
4. Bakshi R, Hutton GJ, Miller JR, et al. 2004. The use of magnetic resonance imaging in the diagnosis and long-term management of multiple sclerosis. Neurology, 63:S3-11.
5. Barde YA. 1997. Help from within for damaged axons. Nature, 385:391-3.
6. Bernard CCA, Mandel TE, MacKay IR. 1992. Experimental models of human autoimmune disease:overview and prototypes. The Autoimmune Diseases II, 47-106.
7. Bornstein MB, Miller AI, Slagle S, et al. 1987. A pilot trial of Cop 1 in exacerbating-remitting multiple sclerosis. N Engl J Med, 317:408-14.
8. Bornstein MB, Miller AI, Slagle S. 1991. A placebo controlled, double blinded, randomized, two-center, pilot trial of Cop 1 in chronic progressive multiple sclerosis. Neurology, 41:533-9.
9. Bornstein MB, Miller AI, Teitelbaum D, et al. 1982. Multiple sclerosis: trial of a synthetic polypeptide. Ann Neurol, 11:317-19.
10. Boneschi FM Rovaris M, Johnson KP, et al. 2003. Effects of glatiramer acetate on relapse rate and accumulated disability in multiple sclerosis: meta-analysis of three double-blinded, randomized, placebo-controlled clinical trials. Mult Scler, 9:349-55.
11. Brenner T, Arnon R, Sela M, et al. 2001. Humoral and cellular immune responses to Copolymer I in MS patients treated with Copaxone. J Neuroimmunol, 115:152-60.
12. Carra A, Onaha P, Sinay V, et al. 2003. A retrospective observational study comparing the four available immunomodulating treatments for RRMS. Eur J Neurol, 10:671-6.
13. Chen M, Gran B, Costell K, et al. 2001. Glatiramer acetate induces a TH2-biased response and crossreactivity with myelin basic protein in patients with MS. Mult Scler, 7:209-19.
14. Comi G, Filippi M, Wolinsky JS; the European/Canadian GA study group. 2001. European/Canadian multicenter, double-blind, randomized, placebo-controlled study of the effects of GA on MRI-measured activity and burden in patients with relapsing multiple sclerosis. Ann Neurol, 49:290-7.
15. Coyle PK, Johnson KP, Pardo L, et al. 2003. Pregnancy outcomes in patients with multiple sclerosis treated with glatiramer acetate (Copaxone) [poster]. Proceedings of the 19th Annual Meeting of the European Committee for Treatment and Research in Multiple Scleroris (ECTRIMS). Milan, Italy. Poster 268
16. Dhib-Jalbut S. 2002. Mechanism of action of interferons and glatiramer acetate in multiple sclerosis. Neurology, 58(Suppl 4):S3-9.
17. Duda PW, Schmied, Cook SL, et al. 2000. Glatiramer acetate (Copaxone) induces degenerate, Th2-polarized immune response in patients with multiple sclerosis. J Clin Invest, 105:967-76.
18. Farina C, Vargas V, Heydari N, et al. 2002. Treatment with glatiramer acetate induces specific IgG4 antibodies in multiple sclerosis patients. J Neuroimmunol, 123:188-92.
19. Filippi M, Rovaris M, Rocca MA, et al. 2001. Glatiramer Acetate reduces the proportion of new MS lesions evolving into "black holes". Neurology, 57:731-3.
20. Fletcher S, Kott E, Steiner-Birmanns B, et al. 2002. Copolymer 1 in relapsing forms of MS: open multicenter study of alternate day administration. Clin Neuropharmacol, 25:11-15.
21. Ford CC, Johnson KP, Lisak RP, et al, The Copaxone Study Group. 2006. A prospective open-label study of glatiramer acetate:over a decade of continuous use in multiple sclerosis patients. Mult Scler, 12:309-20.
22. Ge Y, Grossman RI, Udupa JK, et al. 2000. Glatiramer acetate (Copaxone) treatment in relapsing-remitting MS:Quantitative MR assessment. Neurology, 54:813.
23. Gravel C, Gotz R, Lorrain A, Sendtner M. 1997. Adenoviral gene transfer of ciliary neurotrophic factor and brain-derived neurotrophic factor leads to long-term survival of axotomized motor neurons. Nat Med, 3:765-70.
24. Haas J. 2003. Onset of clinical benefit of glatiramer acetate in 255 patients with RRMS. Proceedings of the 55th Annual Meeting of the American Academy of Neurology. Honolulu, USA. p 06.105.
25. Johnson KP, Brooks BR, Cohen JA, et al. 1995. Copolymer I reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis:results of a phase III multicenter, double-blind placebo-controlled. The Copolymer I Multiple Sclerosis Study Group. Neurology, 45:1268-76.
26. Kerschensteiner M, Stadelmann C, Dechang G, et al. 2003. Neurotrophic cross-talk between the nervous and immune systems: implications for neurological diseases. Ann Neurol, 53:292-304.
27. Khan OH, Tselis AC, Kamholz JA, et al. 2001. A prospective, open label treatment trial to compare the effects of IFNβ-1a, IFNβ-1b, and glatiramer acetate on the relapse rate in RRMS: results after 18 months of therapy. Mult Scler, 7:349-53.
28. Lewin GR, Barde YA. 1996. Physiology of the neurotrophins. Annu Rev Neurosci, 19:289-317.
29. Lobel E, Riven-Kreitman R, Amselem A, et al. 1996. Copolymer-I. Drugs Future, 21:131-4.
30. Mancardi GL, Sardanelli F, Parodi RC, et al. 1998. Effect of copolymer-1 on serial gadolinium-enhanced MRI in relapsing remitting multiple sclerosis. Neurology, 50:1127-33.
31. Martin R, Sturzebecher CS, McFarland HF. 2001. Immunotherapy of multiple sclerosis: where are we? Where should we go? Nat Immunol, 2:785-8.
32. Miller A, Shapiro S, Gershtein R, et al. 1998. Treatment of MS with Copolymer-I (Copaxone):implicating mechanism of Th1 to Th2/Th3 immune-deviation. J Neuroimmunol, 92:113-21.
33. Munari L, Lovati R, Boiko A. 2004. Therapy with glatiramer acetate for multiple sclerosis. Cochrane Database Syst Rev, 1:CD004678.
34. Neuhaus O, Farina C, Wekerle H, et al. 2001. Mechanisms of action of GA in MS. Neurology, 56:702-8.
35. Neuhaus O, Archelos JJ, Hartung H-P. 2003. Immunomodulation in MS: from immunosuppression to neuroprotection. Trends Pharmacol Sci, 24:131-8.
36. Petereit HF, Lindemann H, Schoppe S. 2003. Effect of immunomodulatory drugs on in vitro production of brain-derived neurotrophic factor. Mult Scler, 9:16-20.
37. Prat A, Biernacki K, Antel JP. 2005. Th1 and Th2 lymphocyte migration across the human BBB is specifically regulated by interferon beta and copolymer-1. J Autoimmun, 24:119-24.
38. Rauschka H, Farina C, Sator P, et al. 2005. Severe anaphylactic reaction to glatiramer acetate with specific IgE. Neurology, 64:1481-2.
39. Rovaris M, Comi G, Rocca M, et al; the European/Canadian Glatiramer Acetate Study Group. 2001. Short-term brain volume change in relapsing-remitting multiple sclerosis:effect of glatiramer acetate and implications. Brain, 124:1803-12.
40. Sormani MP, Rovaris M, Valasina P, et al. 2004. Measurement error of two different techniques for brain atrophy assessment in multiple sclerosis. Neurology, 62:1432-4.
41. Teitelbaum D, Meshorer A, Hirshfeld T, et al. 1971. Suppression of experimental allergic encephalomyelitis by a synthetic polypeptide. Eur J Immunol, 1:242-8.
42. Thoenen H. 1995. Neurotrophins and neuronal plasticity. Science, 279:593-8.
43. Trapp BD, Peterson J, Ransohoff RM, et al. 1998. Axonal transaction in the lesions of multiple sclerosis. N Engl J Med, 338:278-85.
44. van Waesberghe JH, van Walderveen MA, Castelijns JA, et al. 1998. Patterns of lesion development in multiple sclerosis; longitudinal observations with T1-weighted spin echo and MTR. AJNR Am J Neuroradiol, 19:675-83.
45. Wolinsky JS. 2004a. Glatiramer acetate for the treatment of multiple sclerosis. Expert Opin Pharmacother, 5:875-91.
46. Wolinsky JS. 2004b. The PROMiSe trial:baseline data review and progress report. Mult Scler, 10(Suppl 1):S65-72.
47. Wolinsky JS, Comi G, Filippi M, et al; the European/Canadian GA Study Group. 2002. Copaxone's effect on MRI-monitored disease in relapsing MS is reproducible and sustained. Neurology, 59:1284-6.
48. Wolinsky JS, Narayana PA, Johnson KP; the Copolymer I Multiple Sclerosis Study Group and the MRI Analysis Center. 2001. United States open-label GA extension trial for relapsing MS: MRI and clinical correlates. Mult Scler, 7:33-41.
49. Wolinsky JS, Pardo L, Stark Y et al; the PROMISE study group. 2004. Effect of GA on primary progressive MS: initial analysis of the completed PROMISE trial. Neurology, 62(Suppl 5):A97-98.
50. Yan Q, Elliott J, Snider WD. 2002. Brain-derived neurotrophic factors rescues spinal motor neurons from axotomy-induced cell death. Nature, 360:753-5.
51. Yong VW. 2002. Differential mechanisms of action of interferon-B and GA in MS. Neurology, 59:802-8.
52. Yousry TA, Major EO, Ryschkewitsch C, et al. 2006. Evaluation of patients treated with natalizumab for progressive multifocal leukoencephalopathy. N Engl J Med, 354:924-33.
53. Ziemssen T, Kumpfel T, Klinkert WEF, et al. 2002. Glatiramer acetate-specific T-helper 1-and 2-type cell lines produce BDNF: implications for multiple sclerosis therapy. Brain, 125:2381-91.