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Key molecule in plant photo-protection identified

Brain cells in a mouse model of Alzheimer's disease have surprised scientists with their ability to recuperate after the disorder's characteristic brain plaques are removed. Researchers at Washington University School of Medicine in St. Louis injected mice with an antibody for a key component of brain plaques, the amyloid beta (Abeta) peptide. In areas of the brain where antibodies cleared plaques, many of the swellings previously observed on nerve cell branches rapidly disappeared.

"These swellings represent structural damage that seemed to be well established and stable, but clearing out the plaques often led to rapid recovery of normal structure over a few days," says senior author David H. Holtzman, M.D., the Charlotte and Paul Hagemann Professor and head of the Department of Neurology. "This provides confirmation of the potential benefits of plaque-clearing treatments and also gets us rethinking our theories on how plaques cause nerve cell damage." Prior to the experiment, Holtzman and some other scientists had regarded plaque damage to nerve cells as a fait accompli--something that the plaques only needed to inflict on nerve cells once. According to Holtzman, the new results suggest that plaques might not just cause damage but also somehow actively maintain it. The study, will appear in the Feb. 5 issue of the Journal of Clinical Investigation. Lead author Robert Brendza, Ph.D., research instructor, began the experiment with one key question: how did clearance of brain plaques, made possible by the development of Abeta antibodies, affect the progression of Alzheimer's disease? Through collaborations with researchers at other institutions, he had acquired several key techniques and technologies that allowed him to closely track changes in live brain cells in mice with an Alzheimer's-like condition. The mice he used for the study had two mutations. One, utilized by scientists at Eli Lilly, causes amyloid plaques to build up, creating the Alzheimer's-like
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