intercellular signaling cascade," said Brandy Wilkinson, the study's lead researcher. Her co-investigators are Jessica Koenigsknecht-Talboo, Christian Grommes, C.Y. Daniel Lee and Gary Landreth from the Alzheimer Research Laboratory in the Case department of neuroscience. Vav also plays a critical role in the initial microglial response to the plaque.

Oxidative damage has long been suspected as playing an early critical role in AD. Because the events that trigger the beginnings of AD are still unknown, the Case researchers began targeting research on the reaction between the plaque and immune cells.

In in vitro studies of brain tissue from mice, the researchers found that the microglia had the appropriate immune response that the plaque was harmful, but then the protein Vav was found to be a component in oxidative damage since elimination of the protein resulted in reduced free radical production.

Wilkinson said by understanding this biological component in the disease process, it holds the potential to "push back the severity of the disease" by developing new drugs that specifically target the component causing the most destruction and decreasing the possibility of injuring or interrupting other biological processes.

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Contact: Susan Griffith
susan.griffith@case.edu
216-368-1004
Case Western Reserve University
18-Jul-2006

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