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2010 Grants - Arispe
Contribution of Alzheimer Abeta Channels to the Abeta-Induced Calcium Response
Nelson Arispe, Ph.D.
The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc.
2010 Investigator-Initiated Research Grant
Beta-amyloid (also known as Abeta), is a protein fragment known to be toxic to nerve cells in the brain. The mechanisms by which beta-amyloid causes such toxicity, however, are not fully understood. One possibility comes from observations that beta-amyloid inserts itself into the membrane of nerve cells and forms channels, thereby allowing toxic amounts of calcium to enter the cell. Although calcium levels need to be high in the blood and fluids of the brain, cells must maintain very low levels of calcium inside in order to survive. Thus, unregulated beta-amyloid channels in the cell membrane could be toxic to the cells.
Nelson Arispe, Ph.D., and colleagues are studying whether channels formed by beta-amyloid in the cell membrane can explain the toxicity of beta-amyloid in nerve cells. They and other scientists have observed that beta-amyloid causes calcium to increase in nerve cells. But it has not been determined whether this effect is due to the formation of membrane channels or to other effects of beta-amyloid. To answer this question, Dr. Arispe's team has developed a series of drugs that block the beta-amyloid membrane channel. They have proposed to use these drugs to determine if such channels can explain the toxicity of beta-amyloid. These studies could provide valuable insights into the toxicity of beta-amyloid, and possibly identify drug candidates for preventing such toxicity.