Research has shown these plaques -- made of beta-amyloid proteins -- to be major players in the disease, although scientists differ on whether the plaques are caused or produced by Alzheimer's.

Previous research at Lilly, led by Dr. Steven M. Paul, has shown repeated doses of a monoclonal antibody compound could prevent deposits of plaques in the brain.

In an effort to reverse symptoms of the disease, Paul and colleagues compared mice with large amounts of plaques to mice of the same age without plaques and younger mice with lower levels of plaques.

They found that after a single injection of the monoclonal antibody m266, the two-year-old mice -- senior citizens in mouse years -- performed as well on two memory tests as the mice that didn't have plaques, and as well as the younger mice.

Results of the research, published in Nature Neuroscience, showed rapid reversal of memory deficits in both object recognition and learning, and memory tasks.

But although memory improved, the levels of plaques did not change, adding to the notion that some types of memory can be improved without reducing the levels of plaque.

Other Sources: Nature Neuroscience