The deposition of amyloid-β (Aβ) peptides into amyloid plaques precedes the cognitive dysfunction of Alzheimer's disease by 10 to 20 years, but they are currently no biomarkers indicative of brain amyloid burden. In March 22 Science, Ronald DeMattos and colleagues from Washington University School of Medicine, St. Louis, US, show that brain to plasma amyloid-β efflux can be used as a measure of brain amyloid load in Alzheimer's disease.

Using a transgenic murine model of Alzheimer's disease, DeMattos et al. injected individuals with a monoclonal antibody to Aβ (m266). They found that after peripheral administration of m266 there was a rapid increase in plasma Aβ and the magnitude of this increase strongly correlated with amyloid burden in the hippocampus and cortex. M266 caused the plasma Aβ increase by both decreasing plasma Aβ degradation and facilitating Aβ efflux from brain to plasma (Science 2002, 295:2264-2267).

"This data...

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