Ab and Neurodegeneration
Accumulation of beta-amyloid (Aβ) protein is thought to be one cause of Alzheimer's disease. Using a genetic model organism (Drosophila melanogaster—also known as the “fruit fly), Dr. Paul Salvaterra and colleagues established a link between Aβ accumulation and abnormal cell maintenance activity, called autophagy. Autophagy maintains cells in a stable, constant condition, as well as protects them from various kinds of stress. Dr. Salvaterra demonstrated that expression in fly brains of one type of beta-amyloid protein, called Aβ42, but not another type, called Aβ40, causes a massive increase in abnormal autophagy activity that appears to lead to neurodegeneration. Counterintuitive to current assumptions about autophagy, Dr. Salvaterra demonstrated that decreased activity results in less Aβ42 accumulation while increased activity seems to contribute to a greater rate of neurotoxicity. These results suggest that Aβ42-dependent abnormal autophagy may be a key cellular event driving neurodegeneration in Alzheimer's disease.
First published on: June 10, 2008
Last modified on: April 12, 2011