Scientists studying the way nerve cells selectively self destruct during embryonic development were surprised to find a protein associated with Alzheimer’s disease is a key factor during early brain development.  This new insight into the brain-destroying disease brings hope that better treatment options might someday be developed that work more effectively than options currently available.

Marc Tessier-Lavigne and his research team were examining the process by which embryonic nerve cells in brain and spinal cord tissue naturally eliminate themselves to make room for a more refined pattern of nerve cell connections.  This mechanism of ‘self-pruning’ is triggered by action from amyloid precursor protein (APP).  In Alzheimer’s disease, enzymes break APP into small pieces of beta amyloid, which is what forms the plaque in an Alzheimer’s patient’s diseased brain.

Tessier-Lavigne, executive vice president of research drug discovery at the biotechnology company, Genentech, Inc., published the findings of this discovery in the journal, ‘Nature.’  He expects further study to determine how and why the APP becomes activated during Alzheimer’s disease and, perhaps better still, how to stop the debilitating brain cell destruction once it starts.

In the United States, about 5.2 million people have Alzheimer’s disease and as many as 26 million people have it around the world.  There is a great deal of research in progress that focuses on removing beta amyloid from the brain but, thus far, nothing has been discovered that significantly alters the course of the disease.  Tessier-Lavigne suggests his discovery of APP’s function in the embryonic brain may direct research attention to APP and the mechanisms by which it works.