Compounds that alter blood levels of beta-amyloid protein in mouse models of Alzheimer's disease represent a potentially safer approach to treating the illness in humans, according to researchers reporting in The Journal of Neuroscience.

Beta-amyloid protein is a component of the amyloid plaques that are found to have accumulated in the brains of Alzheimer patients. Many researchers view beta-amyloid as the underlying cause of the degeneration and dementia.

One effort to develop a vaccine that produced antibodies to beta-amyloid was discontinued a year ago after 15 patients suffered serious brain inflammation (see earlier Alzheimer Week story).

In the new study, researchers injected the beta-amyloid binding agent gelsolin into the peripheral bloodstreams of mice bred to develop Alzheimer's disease.

The brains of mice receiving gelsolin had significantly less beta-amyloid protein, and significantly fewer brain plaques, than those in a genetically similar control group, the researchers reported.

The researchers described their work as an early step in development of "new therapeutic agents that are not limited by the need to penetrate the brain or evoke an immune response."

Other sources: The Journal of Neuroscience