A drug used to prevent relapse of multiple sclerosis can also prevent people at risk from developing the full disease, according to a report published online October 6 by The Lancet. Glatiramer acetate, a synthetic peptide made up of amino acids related to the amino acid composition of myelin basic protein, is currently an approved treatment for people who already have MS. It has been tried, to no avail, in ALS, and a trial for AD is reportedly being planned (see ARF related news story). The current trial asked whether it might prevent, or stave off, disease in people at high risk for MS. Giancarlo Comi of the University Vita-Salute in Milan, Italy, and colleagues reported on the multicenter trial.

For many people with MS, their initial brush with disease was a single episode, with symptoms suggestive of central nervous system lesions, that usually dissipates. Known as clinically isolated syndrome, these events can be the harbinger of a later MS diagnosis, although that is not always the case. The researchers in the PreCISe (Presenting with a Clinically Isolated Syndrome) study group, encompassing doctors at 80 sites in 16 countries, recruited 481 subjects who experienced such an isolated event. The study was funded by Teva Pharmaceutical Industries of Israel, which makes and markets glatiramer acetate as Copaxone.

Study participants received either 20 milligrams of Copaxone via injection daily or a placebo. The researchers found that those on the glatiramer acetate treatment had a 45 percent reduced risk of converting to full MS, compared to the placebo group, over the three years of the trial. Of those participants who did progress to MS, those in the Copaxone group took more than twice as long (772 days) than placebo recipients (336 days) to do so.—Amber Dance


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News Citations

  1. ALS: T Cells Step Up

Further Reading


  1. . Are there protective treatments for cognitive decline in MS?. J Neurol Sci. 2006 Jun 15;245(1-2):183-6. PubMed.
  2. . Nasal vaccination with a proteosome-based adjuvant and glatiramer acetate clears beta-amyloid in a mouse model of Alzheimer disease. J Clin Invest. 2005 Sep;115(9):2423-33. PubMed.
  3. . Neuroprotection and neurogeneration in MS and its animal model EAE effected by glatiramer acetate. J Neural Transm. 2009 Nov;116(11):1443-9. PubMed.
  4. . Glatiramer acetate-reactive T cells produce brain-derived neurotrophic factor. J Neurol Sci. 2003 Nov 15;215(1-2):37-44. PubMed.
  5. . Randomized controlled phase II trial of glatiramer acetate in ALS. Neurology. 2006 Apr 11;66(7):1117-9. PubMed.
  6. . Glatiramer acetate could be a potential therapeutic agent for Parkinson's disease through its neuroprotective and anti-inflammatory effects. Med Hypotheses. 2007;69(6):1219-21. PubMed.
  7. . Glatiramer acetate fights against Alzheimer's disease by inducing dendritic-like microglia expressing insulin-like growth factor 1. Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11784-9. PubMed.
  8. . On the horizon: possible neuroprotective role for glatiramer acetate. Mult Scler. 2004 Jun;10 Suppl 1:S81-6; discussion S86-9. PubMed.
  9. . Dual action of glatiramer acetate (Cop-1) in the treatment of CNS autoimmune and neurodegenerative disorders. Trends Mol Med. 2002 Jul;8(7):319-23. PubMed.

Primary Papers

  1. . 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. PubMed.