Glatiramer acetate in multiple sclerosis

References

• Compston A, Matthews WB, Lassmann H, Ebers G, Wekerle H. McAlpine’s Multiple Sclerosis, Third Edition. Churchill Livingstone, NY, USA (1998).
   Google Scholar
• Poser CM. The epidemiology of multiple sclerosis: a general overview. Ann. Neurol. 36(Suppl. 2), S180–S193 (1994).
   PubMed Web of Science ®Google Scholar
• Lublin FD, Reingold SC. Defining the clinical course of multiple sclerosis: results of an international survey. National MS Society (USA) Advisory Committee on Clinical Trials of New Agents in Multiple Sclerosis. Neurology 46, 907–911 (1996).
   PubMed Web of Science ®Google Scholar
• Lublin FD, Baier M, Cutter G. Effect of relapses on development of residual deficit in multiple sclerosis. Neurology 61(11), 1528–1532 (2003).
   PubMed Web of Science ®Google Scholar
• Confavreux C, Vukusic S, Moreau T, Adeleine P. Relapse and progression of disability in multiple sclerosis. N. Engl. J. Med. 343, 1430–1438 (2000).
   PubMed Web of Science ®Google Scholar
• Thompson AJ, Polman CH, Miller DH et al. Primary progressive multiple sclerosis. Brain 120, 1085–1096 (1997).
   PubMed Web of Science ®Google Scholar
• Steinman L. Multiple sclerosis: a two-stage disease. Nature Immunol. 2(9), 762–764 (2001).
   PubMed Web of Science ®Google Scholar
• Lucchinetti C, Bruck W, Noseworthy J. Multiple sclerosis: recent developments in neuropathology, pathogenesis, magnetic resonance imaging studies and treatment. Curr. Opin. Neurol. 14(3), 259–269 (2001).
   PubMed Web of Science ®Google Scholar
• Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mork S, Bo L. Axonal transection in the lesions of multiple sclerosis. N. Engl. J. Med. 338(5), 278–285 (1998).
   PubMed Web of Science ®Google Scholar
• Miller D, Barkhof F, Montalban X, Thompson A, Filippi M. Clinically isolated syndromes suggestive of multiple sclerosis, Part I: natural history, pathogenesis, diagnosis, and prognosis. Lancet Neurol. 4(5), 281–288 (2005).
   PubMed Web of Science ®Google Scholar
• Inglese M, Benedetti B, Filippi M. The relation between MRI measures of inflammation and neurodegeneration in multiple sclerosis. J. Neurol. Sci. 233, 15–19 (2005).
   Google Scholar
• Filippi M, Rovaris M, Inglese et al. Interferon β1a for brain tissue loss in patients at presentation with syndromes suggestive of multiple sclerosis: a randomised, double-blind, placebo-controlled trial. Lancet 364(9444), 1489–1496 (2004).
   PubMed Web of Science ®Google Scholar
• Hemmer B, Archelos JJ, Hartung HP. New concepts in the immunopathogenesis of multiple sclerosis. Nature Rev. Neurosci. 3(4), 291–301 (2002).
   PubMed Web of Science ®Google Scholar
• Comi G. Why treat early multiple sclerosis patients? Curr. Opin. Neurol. 13(3), 235–240 (2000).
   PubMedGoogle Scholar
• Weiner H. Immunosuppressive treatment in multiple sclerosis. J. Neurol. Sci. 223, 1–11 (2004).
   PubMed Web of Science ®Google Scholar
• Trapp BD, Ransohoff R, Rudick R. Axonal pathology in multiple sclerosis: relationship to neurologic disability. Curr. Opin. Neurol. 12(3), 295–302 (1999).
   PubMed Web of Science ®Google Scholar
• Filippi M, Bozzali M, Rovaris M et al. Evidence for widespread axonal damage at the earliest clinical stage of multiple sclerosis. Brain 126(2), 433–437 (2003).
   PubMed Web of Science ®Google Scholar
• Bjartmar C, Trapp BD. Axonal and neuronal degeneration in multiple sclerosis: mechanisms and functional consequences. Curr. Opin. Neurol. 14(3), 271–278 (2001).
   PubMed Web of Science ®Google Scholar
• Schwartz M, Kipnis J. Multiple sclerosis as a by-product of the failure to sustain protective autoimmunity: a paradigm shift. Neuroscientist 8(5), 405–413 (2002).
   PubMedGoogle Scholar
• Hauben E, Nevo U, Yoles E et al. Autoimmune T-cells as potential neuroprotective therapy for spinal cord injury. Lancet 355(9200), 286–287 (2000).
   PubMedGoogle Scholar
• Moalem G, Leibowitz-Amit R, Yoles E, Mor F, Cohen IR, Schwartz M. Autoimmune T-cells protect neurons from secondary degeneration after central nervous system axotomy. Nature Med. 5(1), 49–55 (1999).
   PubMed Web of Science ®Google Scholar
• Kerschensteiner M, Stadelmann C, Dechant G, Wekerle H, Hohlfeld R. Neurotrophic cross-talk between the nervous and immune systems: implications for neurological diseases. Ann. Neurol. 53(3), 292–304 (2003).
   PubMed Web of Science ®Google Scholar
• Stadelmann C, Kerschensteiner M, Misgeld T, Bruck W, Hohlfeld R, Lassmann H. BDNF and gp145trkB in multiple sclerosis brain lesions: neuroprotective interactions between immune and neuronal cells? Brain 125(1), 75–85 (2002).
   PubMed Web of Science ®Google Scholar
• Martino G, Adorini L, Rieckmann P et al. Inflammation in multiple sclerosis: the good, the bad, and the complex. Lancet Neurol. 1(8), 499–509 (2002).
   PubMed Web of Science ®Google Scholar
• Neuhaus O, Kieseier BC, Hartung HP. Mitoxantrone (Novantrone) in multiple sclerosis: new insight. Expert Rev. Neurotherapeutics 4, 17–26 (2004).
   PubMedGoogle Scholar
• Jacobs LD, Beck RW, Simon JH et al. Intramuscular interferon beta-1a therapy initiated during a first demyelinating event in multiple sclerosis. CHAMPS Study Group. N. Engl. J. Med. 343(13), 898–904 (2000).
   PubMed Web of Science ®Google Scholar
• Comi G, Filippi M, Barkhof F et al. Early Treatment of Multiple Sclerosis Study Group. Effect of early interferon treatment on conversion to definite multiple sclerosis: a randomised study. Lancet 357(9268), 1576–1582 (2001).
   Google Scholar
• Teitelbaum D, Meshorer A, Hirshfeld T, Arnon R, Sela M. Suppression of experimental allergic encephalomyelitis by a synthetic polypeptide. Eur. J. Immunol. 1(4), 242–248 (1971).
   Google Scholar
• Arnon R. The development of Cop 1 (Copaxone), an innovative drug for the treatment of multiple sclerosis: personal reflections. Immunol. Lett. 50(1–2), 1–15 (1996).
   PubMed Web of Science ®Google Scholar
• Fridkis-Hareli M, Neveu JM, Robinson RA et al. Binding motifs of copolymer 1 to multiple sclerosis- and rheumatoid arthritis-associated HLA-DR molecules. J. Immunol. 162(8), 4697–4704 (1999).
   PubMed Web of Science ®Google Scholar
• Smith KJ, Pyrdol J, Gauthier L, Wiley DC, Wucherpfennig KW. Crystal structure of HLA-DR2 (DRA*0101, DRB1*1501) complexed with a peptide from human myelin basic protein. J. Exp. Med. 188(8), 1511–1520 (1998).
   PubMed Web of Science ®Google Scholar
• Arnon R, Sela M. Immunomodulation by the copolymer glatiramer acetate. J. Mol. Recognit. 16(6), 412–421 (2003).
   Google Scholar
• Arnon R, Sela M, Teitelbaum D. New insights into the mechanism of action of copolymer 1 in experimental allergic encephalomyelitis and multiple sclerosis. J. Neurol. 243(4 Suppl. 1), S8–S13 (1996).
   Google Scholar
• Aharoni R, Teitelbaum D, Arnon R, Sela M. Copolymer 1 acts against the immunodominant epitope 82–100 of myelin basic protein by T-cell receptor antagonism in addition to major histocompatibility complex blocking. Proc. Natl Acad. Sci. 96(2), 634–639 (1999).
   Google Scholar
• Neuhaus O, Farina C, Wekerle H, Hohlfeld R. Mechanisms of action of glatiramer acetate in multiple sclerosis. Neurology 56(6), 702–708 (2001).
   PubMed Web of Science ®Google Scholar
• Chen M, Gran B, Costello K, Johnson K, Martin R, Dhib-Jalbut S. Glatiramer acetate induces a Th2-biased response and crossreactivity with myelin basic protein in patients with MS. Mult. Scler. 7, 209–219 (2001).
   PubMed Web of Science ®Google Scholar
• Brenner T, Arnon R, Sela A et al. Humoral and cellular immune responses to Copolymer 1 in multiple sclerosis patients treated with Copaxone. J. Neuroimmunol. 115, 152–160 (2001).
   PubMed Web of Science ®Google Scholar
• Biernacki K, Prat A, Blain M, Antel JP. Regulation of Th1 and Th2 lymphocyte migration by human adult brain endothelial cells. J. Neuropathol. Exp. Neurol. 60, 1127–1136 (2001).
   PubMed Web of Science ®Google Scholar
• Kreitman RR, Blanchette F. On the horizon: possible neuroprotective role for glatiramer acetate. Mult. Scler. 10, S81–S89 (2004).
   Google Scholar
• Ziemssen T, Kumpfel T, Klinkert WE, Heuhaus O, Hohlfeld R. Glatiramer acetate-specific T-helper 1- and 2-type cell lines produce BDNF: implications for multiple sclerosis therapy. Brain-derived neurotrophic factor. Brain 125, 2381–2391 (2002).
   PubMed Web of Science ®Google Scholar
• Johnson KP, US Phase III Copolymer 1 Study Group. Antibodies to copolymer 1 do not interfere with its clinical effect. Ann. Neurol. 38, 973 (1995).
   Google Scholar
• Teitelbaum D, Brenner T, Abramsky O et al. Antibodies to glatiramer acetate do not interfere with its biological functions and therapeutic efficacy. Mult. Scler. 9, 592–599 (2003).
   PubMed Web of Science ®Google Scholar
• Salama HH, Hong J, Zang YCQ, El-Mongui A, Zhang J. Blocking effects of serum reactive antibodies induced by glatiramer acetate treatment in multiple sclerosis. Brain 126, 2638–2647 (2003).
   PubMed Web of Science ®Google Scholar
• Bornstein M, Miller A, Slagle S et al. A pilot trial of GA in exacerbating-remitting multiple sclerosis. N. Engl. J. Med. 317, 408–414 (1987).
   PubMed Web of Science ®Google Scholar
• Johnson KP, Brooks BR, Cohen JA et al. Copolymer 1 reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis: results of a phase III multicenter, double-blind placebo-controlled trial. The Copolymer 1 Multiple Sclerosis Study Group. Neurology 45(7), 1268–1276 (1995).
   PubMed Web of Science ®Google Scholar
• Johnson KP, Brooks BR, Cohen JA et al. Extended use of glatiramer acetate (Copaxone) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability. Copolymer 1 Multiple Sclerosis Study Group. Neurology 50(3), 701–708 (1998).
   PubMed Web of Science ®Google Scholar
• Comi G, Filippi M, Wolinsky JS. European/Canadian multicenter, double-blind, randomized, placebo-controlled study of the effects of glatiramer acetate on magnetic resonance imaging-measured disease activity and burden in patients with relapsing multiple sclerosis. European/Canadian Glatiramer Acetate Study Group. Ann. Neurol. 49(3), 290–297 (2001).
   PubMed Web of Science ®Google Scholar
• Martinelli Boneschi F, Rovaris M, Johnson KP et al. Effects of glatiramer acetate on relapse rate and accumulated disability in multiple sclerosis: meta-analysis of three double-blind, randomized, placebo-controlled clinical trials. Mult. Scler. 9(4), 349–355 (2003).
   Google Scholar
• Wolinsky JS, Johnson KP, Comi G et al. The effects of glatiramer acetate on sustained accumulated disability in relapsing multiple sclerosis are evident within one year: meta-analysis results of three double blind, placebo-controlled trials. Proceedings of the 19th Annual Meeting of the European Committee for Treatment and Research in MS (ECTRIMS), Milan, Italy (2003) (Abstract 487).
   Google Scholar
• Johnson KP, Brooks BR, Ford CC et al. Glatiramer acetate (Copaxone): comparison of continuous versus delayed therapy in a six-year organized multiple sclerosis trial. Mult. Scler. 9, 585–591 (2003).
   PubMed Web of Science ®Google Scholar
• Johnson KP, Ford CC, Lisak RP et al. Neurologic consequence of delaying glatiramer acetate therapy for multiple sclerosis: 8-year data. Acta Neurol. Scand. 111, 42–47 (2005).
   PubMed Web of Science ®Google Scholar
• Wolinsky JS for the PROMiSe Trial Study Group. The PROMiSe trial: baseline data review and progress report. Mult. Scler. 10(Suppl. 1), S65–S72 (2004).
   PubMedGoogle Scholar
• Wolinsky JS, Pardo L, Stark Y et al. and the PROMiSe Study Group. Effect of glatiramer acetate on primary progressive multiple sclerosis: initial analysis of the completed PROMiSe trial. Neurology 62(Suppl. 5), A97–A98 (2004).
   Google Scholar
• Mancardi GL, Sardanelli F, Parodi RC et al. Effect of copolymer-1 on serial gadolinium-enhanced MRI in relapsing remitting multiple sclerosis. Neurology 50(4), 1127–1133 (1998).
   PubMed Web of Science ®Google Scholar
• Ge Y, Grossman RI, Udupa JK et al. Glatiramer acetate (Copaxone) treatment in relapsing-remitting MS: quantitative MR assessment. Neurology 54(4), 813–817 (2000).
   PubMed Web of Science ®Google Scholar
• Wolinsky JS, Narayana PA, Johnson KP. United States open-label glatiramer acetate extension trial for relapsing multiple sclerosis: MRI and clinical correlates. Multiple Sclerosis Study Group and the MRI Analysis Center. Mult. Scler. 7(1), 33–41 (2001).
   PubMed Web of Science ®Google Scholar
• Wolinsky JS, Comi G, Filippi M, Ladkani D, Kadosh S, Shifroni G (European/Canadian Glatiramer Acetate Study Group). Copaxone’s effect on MRI-monitored disease in relapsing MS is reproducible and sustained. Neurology 59(8), 1284–1286 (2002).
   PubMed Web of Science ®Google Scholar
• Filippi M, Rovaris M, Capra R et al. A multi-centre longitudinal study comparing the sensitivity of monthly MRI after standard and triple dose gadolinium-DTPA for monitoring disease activity in multiple sclerosis. Implications for Phase II clinical trials. Brain 121, 2011–2020 (1998).
   PubMed Web of Science ®Google Scholar
• Rovaris M, Codella M, Moiola L et al. Effect of glatiramer acetate on MS lesions enhancing at different gadolinium doses. Neurology 59(9), 1429–1432 (2002).
   PubMed Web of Science ®Google Scholar
• Filippi M, Rovaris M, Rocca MA, Sormani MP, Wolinsky JS, Comi G and the European/Canadian Glatiramer Acetate Study Group. Glatiramer acetate reduces the proportion of new MS lesions evolving to black holes. Neurology 57, 731–733 (2001).
   PubMed Web of Science ®Google Scholar
• Wolinsky JS, Narayana PA, Johnson KP. United States open-label glatiramer acetate extension trial for relapsing multiple sclerosis: MRI and clinical correlates. Multiple Sclerosis Study Group and the MRI Analysis Center. Mult. Scler. 7(1), 33–41 (2001).
   PubMed Web of Science ®Google Scholar
• Rovaris M, Comi G, Rocca MA, Wolinsky JS, Filippi M (European/Canadian Glatiramer Acetate Study Group). Short-term brain volume change in relapsing-remitting multiple sclerosis: effect of glatiramer acetate and implications. Brain 124, 1803–1812 (2001).
   PubMed Web of Science ®Google Scholar
• Sormani MP, Rovaris M, Valsasina P, Wolinsky JS, Comi G, Filippi M. Measurement error of two different techniques for brain atrophy assessment in multiple sclerosis. Neurology 62(8), 1432–1434 (2004).
   PubMed Web of Science ®Google Scholar
• Khan OA, Tselis AC, Kamholz JA, Garbern JY, Lewis RA, Lisak RP. A prospective, open-label treatment trial to compare the effect of IFN β1a (Avonex), IFN β1b (Betaseron), and glatiramer acetate (Copaxone) on the relapse rate in relapsing-remitting multiple sclerosis. Eur. J. Neurol. 8, 141–148 (2001).
   Google Scholar
• Khan OA, Tselis AC, Kamholz JA, Garbern JY, Lewis RA, Lisak RP. A prospective, open-label treatment trial to compare the effect of IFN β1a (Avonex), IFN β1b (Betaseron), and glatiramer acetate (Copaxone) on the relapse rate in relapsing-remitting multiple sclerosis: results after 18 months of therapy. Mult. Scler. 7, 349–353 (2001).
   PubMed Web of Science ®Google Scholar
• Carra A, Onaha P, Sinay V et al. A retrospective observational study comparing the four available immunomodulatory treatments for relapsing-remitting multiple sclerosis. Eur. J. Neurol. 10, 671–676 (2003).
   PubMed Web of Science ®Google Scholar
• Mancardi GL, Murialdo A, Drago F et al. Localized lipoatrophy after prolonged treatment with copolymer 1. J. Neurol. 247(3), 220–221 (2000).
   PubMed Web of Science ®Google Scholar
• Hwang L, Orengo I. Lipoatrophy associated with glatiramer acetate injections for the treatment of multiple sclerosis. Cutis 68(4), 287–288 (2001).
   PubMed Web of Science ®Google Scholar
• Coyle PK, Johnson KP, Pardo L, Stark Y. Pregnancy outcomes in patients with multiple sclerosis treated with glatiramer acetate (Copaxone). Proceedings of the 19th Annual Meeting of the European Committee for Treatment and Research in MS (ECTRIMS). Milan, Italy (2003) (Abstract 268).
   Google Scholar