One of the mysteries of Alzheimer dementia (AD) has been the normal function of the amyloid precursor protein (APP);  these specialized proteins are concentrated at the points where neurons connect within the brain. Even though the sticky amyloid plaques (which have been viewed as a hallmark sign of AD) result from APP, it seems unlikely that APP exists simply to cause AD. In a recent study, scientists from the U.S. and France show that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for AD, their symptoms were reversed, and the sticky amyloid was reduced.

These results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong; instead, it is beginning to appear that the disease stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections — both by binding to APP and activating normal cell functional programs.  One thing about novel molecular nanoresearch is that it always keeps things interesting. | LINK

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