Referenser
[1] Johnson K 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, Neurology 1998; 50:701-708.
[2] Khan O et al., Effect of disease-modifying treatment on brain athrophy in early and mildly affected RRMS over a long-term period: Results of a five-year study. Presented at ECTRIMS, Prague, 2007, P03
[3] Filippi M et al., Glatiramer acetate reduces the porpotion of new MS lesions evolving into ”black holes”, Neurology 2001; 57:731-733,
[4] Khan O et al., Axonal metabolic recovery and potential neuroprotective effect of glatiramer acetat in relapsing-remitting multiple sclerosis, Multiple Sclerosis 2005; 11:646-651
[5] Ford CC et al., A prospective open-label study of glatiramer acetat: over a decade of continous use in multiple sclerosis patients, Mult Scler 2006; 12:309-320.
[6] Brenner T et al., Humoral and cellular immune responses to Copolymer 1 in multiple sclerosis patients treated with Copaxone, J Neuroimmunology 2001; 115: 152-160,
[7] Teitelbaum D et al., Antibodies to glatiramer acetat do not interfere with its biological functions and therapeutic efficacy, Mult Scler 2003; 9: 592-599
[8] Haas J and Firzlaff M., Twenty-four-month comparison of immunomodulatory treatments – a retrospective open label study in 308 RRMS patients treated with beta interferons or glatiramer acetat, Eur J Neurol. 2005; 12:425-431,
[9] www.FASS.se
[10] IFNB Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group. Neurology 1995; 45(7):1277-1285
[11] Jacobs LD, et al., Intramuscular interferon Beta-1a for disease progression in relapsing multiple sclerosis, Ann Neurol. 1996; 39(3):285-294
[12] PRISMS Study Group and The University of British Columbia MS/MRI Analysis Group. Neurology 2001; 56:1628-1636
[13] Zwibel HL et al., Glatiramer acetat in treatment-naïve and prior interferon-B-1b treated multiple sclerosis patients, Acta Neurol Scand. 2006;113 (6):378-86
[14] Caon C et al., Clinical course after change of immunomodulating therapy in relapsing-remitting multiple sclerosis, Eur J Neurol. 2006;13 (5):471-474.
[15] Bermel R. A et al., The measurement and clinical relevance of brain atrophy in multiple sclerosis, Lancet Neurology 2006;5: 158-70
[16] Vega José A. et al Neutrophins and the immune system, J Anat., 2003, 203, 1-19
[17] O´Connor P et al., IFN-ß 1b 500 μg, IFN-ß 1b 250 μg and glatiramer acetate: primary outcomes of the BEYOND study. Presented at a late breaking sesion, AAN, Chicago 2008 (LBS.004)
[18] Tallantyre E. C.et al., Greater loss of axons in primary progressive multiple sclerosis plaques compared to secondary progressive disease, Brain, 2009:132; 1190-1199
[19] Azoulay D et al. Lower brain-derived neutrophic factor in serum of relapsing remitting MS: reversal by glatiramer acetate, J. Neuroimmmunology 2005; 167:215-218
[20] Ziemssen T et al., Glatiramer acetat-specific T-helper 1- and 2-type cell lines produce BDNF: implications for multiple sclerosis therapy, Brain 2002; 125:2381-2391
[21] Barkhof F et al., MRI in multiple sclerosis: correlation with expanded disability status scale, Multiple Sclerosis, 1999, aug 5 (4): 283-6
[22] Sørensen PS et al., Guidelines on use of anti-INF-b antibody measurement in multiple sclerosis: report of an EFNS Task Force on IFN-b antibodies in multiple sclerosis, Eur J Neurol. 2005; 12(11): 817-27
[23] Svenska MS-sällskapets Metodbok,. Se www.mssallskapet.se
[24] Arnold L. Douglas, Treatment with glatiramer acetate protects axons in patients in clinically isolated syndromes: evidence from the PreCISe trial, Multiple Sclerosis, volume 14, supplement 1, s 10, 2008
[25] Schrempf W et al., Glatiramer acetat: mechanisms of action in multiple sclerosis, Autoimmun Rev. 2007 Aug; 6(7):469-75.
[26] O’Connor P et al. IFN-ß 1b 500μg, IFN-ß 1b 250μg and glatiramer acetate in relapsing-remitting multiple sclerosis: a prospective, randomised, multicentre study (BEYOND). Lancet Neurology 2009; 2009; 8: 889-97
[27] Mikol D et al. Comparison of subcutaneous interferon beta 1a with glatiramer acetate in patients with relapsing multiple sclerosis (REGARD): a multicentre, randomised, parallel, open-label trial. Lancet Neurology 2008; 7:903-914 .
[28] Cadavid D, et al., Efficacy of treatment of MS with IFN-1b or glatiramer acetat by monthly brain MRI in the BECOME study, Neurology 2009; 72:1976-1983
[29] Wolansky L. et al. Betaseron vs COPAXONE in MS with Triple-dose Gadolinium and 3-T MRI Endpoints (BECOME); Annoncement of the Final Primary Study Outcome. Presented at ECTRIMS, Prague 2007, P206.
[30] Thrower B.W., Clinically isolated syndromes: Predicting and delaying multiple sclerosis, Neurology 2007; 68 (suppl 4):S12-S15.
[31] Mofett JR., N-Acetylaspartate in the CNS: from neurodiagnostics to neurobiologi, Prog Neurobiol, 2007, Feb; 81(2):89-131
[32] Miller JR., The importance of early diagnosis of multiple sclerosis, J Manag Care Pharm. 2004 Jun; 10(3 suppl B):S4-11.
[33] Comi G. Effect of glatiramer acetate on conversion to clinically definite multiple sclerosis in patients with clinically isolated syndrome (PreCISe study): a randomised, double-blind, placebo-controlled trial, Lancet, 2009, Oct 31; 374 (9700): 1503-11. E-pub 2009 Oct 6
[34] Rocca, M. Treatment with glatiramer acetate reduces T1 and T2-weighted magnetic resonance imaging activity in patients with clinically
isolated syndrome suggestive of MS, Presented at WCTRIMS 2008, Montreal, Canada. P501.


