Researchers at Genentech of South San Francisco and the Salk Institute of La Jolla have discovered a new mechanism of nerve-cell death that might lead to brain deterioration in Alzheimer’s disease. The finding opens doors to potential treatment for the disease, a condition that has no cure at the moment, as existent drugs only seem to alleviate its symptoms.

 

“The key player we’re focusing on is a protein called APP [amyloid precursor protein]. We know that APP is a bad actor in Alzheimer’s, but it has been unclear how it participates,” said Marc Tessier-Lavigne, executive vice president of research drug discovery at Genentech. His study appears in the journal Nature.

 

It appears that two components of APP can cause nerve cells to self-destruct: the amyloid beta peptide, which collects in abnormal plaques in the brain that are a diagnostic sign of the disease and the N fragment or N-APP, which was found to trigger a chain of events that also destroys neurons, the study says.

 

“Now, instead of having one dog in the race, there are two. It’s a very exciting paper. It’s going to have a major impact on research in the Alzheimer’s filed,” said Paul Greengard, a professor at the Rockefeller University in New York, whose work on nerve cell communication brought him the Nobel Prize in physiology or medicine in 2000.

 

It’s true the research is in its incipient stage being based on laboratory and mouse experiments, but, if the same mechanism is found on adults’ brain as well, the discovery may offer new targets for drug development to slow degenerative brain diseases, Tessier-Lavigne said.