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FOCUS ON RESEARCH Previous Volume 361:1041-1043 September 10, 2009 Number 11 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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When progressive multifocal leukoencephalopathy (PML), a rare demyelinating disease induced by JC virus, appeared in 2004 as a complication of natalizumab treatment for multiple sclerosis, a more common demyelinating disease, it seemed an odd twist of nature. PML had never been reported in patients with multiple sclerosis, and to find patients who simultaneously had two demyelinating diseases with very different origins and pathologic characteristics was a dramatic surprise.

Natalizumab, a humanized monoclonal antibody that binds to the ₄ integrin molecule at the β1 and β7 epitopes, is an adhesion-molecule inhibitor that prevents extravasation of T and B cells into the brain . . . [Full Text of this Article]

Source Information

From the Laboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, Bethesda, MD.

This article has been cited by other articles:

• (2009). Plasmapheresis for Managing Natalizumab-Associated PML: A Risky Proposition. JWatch Neurology 2009: 1-1 [Full Text]