2003 Investigator-Initiated Research Grant

The current understanding of Alzheimer’s disease is that a number of destructive processes are occurring at once, all possibly set in motion by the abnormal protein fragment beta-amyloid. Many scientists believe that chronic inflammatory activity is one of these processes. In the brain, inflammation is partially controlled by cells called glia, whose primary role is to support and nourish nerve cells, the primary information-processing cells of the nervous system. During inflammatory responses, glia release various molecules designed to attack foreign substances such as viruses and bacteria. If released over long periods, these inflammatory molecules can become toxic to nerve cells.

James McLarnon, PhD, and colleagues have found preliminary evidence that glia release inflammatory molecules in response to stimulation by beta-amyloid. They hypothesize that calcium is one of the critical intermediaries inside the glia that helps convey the message from beta-amyloid to produce and release these toxic molecules. Working in cultured human glia, the researchers are going to test several drugs known to interfere with calcium, in the hope they will block the signal from beta-amyloid. If successful, this strategy might offer a way to protect nerve cells from inflammatory molecules.