Amyloid beta plaques, a hallmark of Alzheimer's disease, can be prevented by interacting with the protein cystatin C, U.S. and German researchers have found.

Lead author Efrat Levy of the New York University School of Medicine said two animal studies may open the door to new treatments for Alzheimer's disease that mimic the effects of cystatin C.

The first study, by Levy and researchers at the Nathan S. Kline Institute for Psychiatric Research and New York University School of Medicine, and the second study with Levy and colleagues in the laboratory of Dr. Mathias Jucker at the Hertie-Institute for Clinical Brain Research in Tubingen, Germany, used genetically engineered mice to produce human cystatin C and abundant amounts of amyloid beta plaques in their brains.

The protein cystatin C bound to the soluble, non-pathological form of amyloid beta in these mice, and inhibited the aggregation and deposition of amyloid beta plaques in the brain, Levy said.

Both studies are published online in advance of the December print issue of the journal Nature Genetics.  // Copyright 2007 by United Press International



Publication date: 20 November 2007   

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