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Joan Stephenson, PhD

JAMA. 2002;287:2937.

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

An experimental drug that depletes the body of a protein that helps anchor damaging deposits of amyloid protein in tissues may provide a new therapeutic approach for amyloidosis and other disorders (such as Alzheimer disease) in which amyloid is present, according to new findings in the May 16 issue of Nature.

In amyloidosis, abnormally folded protein is deposited as insoluble fibrils that lead to tissue damage and disease. Another protein, serum amyloid P component (SAP), binds to amyloid fibrils and makes them particularly resistant to degradation by the body.

A team of researchers from England, Switzerland, and Japan identified a compound—a small-molecule drug called CPHPC—that interferes with SAP binding to amyloid fibrils and leads to rapid clearance of SAP by the liver. In studies of mice with an experimentally induced form of amyloidosis, the researchers found that animals treated with the anti-SAP compound had significantly less amyloid . . . [Full Text of this Article]