A molecule expressed by nerve cells may protect against Alzheimer's disease by reducing the risk of plaque formation in the brain. In Alzheimer's disease, protein plaques in the brain accumulate. They are derived from the amyloid precursor protein (APP). It is chopped into smaller fragments including amyloid beta peptide. Amyloid beta forms plaques that destroy nerve cells.

Thomas Willnow of the Max Delbrück Center for Molecular Medicine (MDC) and colleagues have now shown that a molecule called sorLa (for "sorting protein-related receptor"), binds to APP in nerve cells and prevents its dissection into amyloid beta peptide.

They have also shown that genetically modified mice that can't produce sorLA have increased levels of amyloid beta peptide.

And in the brain of patients who died from Alzheimer's, nerve cells had not produced sorLA while the nerve cells of a control group had.

The researchers conclude that producing little or no sorLA in the brain is linked with uncontrolled production of amyloid beta peptide and a likely acceleration of onset and progression of neurodegenerative processes.

Research is now directed towards finding substances that can increase production of sorLA in the brain.

SOURCE: Proceedings of the National Academy of Sciences.