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Johann Sellner, MD; Isabell Greeve, MD; Stephen L. Leib, MD; Heinrich P. Mattle, MD

Arch Neurol. 2008;65(5):672-674.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Interferon beta, the current cornerstone of multiple sclerosis (MS) therapy, was shown to reduce the ratio of matrix metalloproteinase 9 (MMP-9)–tissue inhibitor of metalloproteinase 1 (TIMP-1) in order to attenuate overactive proteolysis and inhibit leukocyte migration.^1-3 Matrix metalloproteinases, a family of extracellular matrix-degrading enzymes, are involved in the pathogenesis of MS by facilitating leukocyte migration, disruption of the blood-brain barrier, processing of cytokines and their receptors, and demyelination.¹

Immunomodulatory properties of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, including atorvastatin, may be beneficial for the treatment of MS. Among the immunomodulatory effects proposed for statins, increased attention is drawn to the modulation of MMPs. In vitro results suggest that statins may increase MMP-9 activity and disrupt the proteolytic balance restored by interferon beta.^{1, 4}

In this study, we aimed to evaluate the treatment effects of interferon beta alone and . . . [Full Text of this Article]

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