Matrix metalloproteinases in inflammatory demyelination - Targets for treatment

Matrix metalloproteinases (MMPs) degrade all protein components of the extr acellular matrix. Functionally, they contribute to several different physio logic conditions, such as angiogenesis or bone remodeling, as well as patho logic conditions in humans, such as rheumatoid arthritis and tumor growth. MMPs seem to be important in the pathogenesis of inflammatory demyelinating diseases of the central and peripheral nervous system, especially in MS an d in Guillain-Barre syndrome (GBS). Key mechanisms in the genesis of inflam matory demyelination, such as leukocyte recruitment, blood-brain barrier or blood-nerve barrier breakdown, myelin destruction, and release of disease- promoting cytokines, are considered to be MMP-dependent processes. In exper imental autoimmune encephalomyelitis, an animal model of MS, and experiment al autoimmune neuritis, an animal model of GBS, different synthetic inhibit ors targeting MMP activity are able to suppress and even reverse ongoing di sease. This evidence points to MMPs as new targets for treatment in inflamm atory demyelination.