In genetic studies involving some 6,000 volunteers, the researchers discovered that variants of the gene SORL1 were more common in people with late-onset Alzheimer's than in healthy people the same age.

The Alzheimer's victims also had a strikingly low level of the SORL1 protein in the blood compared with healthy people -- less than 50 percent of the level seen in the healthy group.

In healthy people, SORL1, which is a "traffic cop" regulating the flow of amyloid precursor protein (APP) inside nerve cells in the brain, drives the protein to a part of the cell where it is recycled.

But in people with the gene variants, the gene appears to drive APP to another region of the cell where it accumulates and is degraded into amyloid plaques -- the abnormal sticky proteins that gum up the brain of Alzheimer's victims, the researchers said, citing laboratory experiments.

"The importance of the finding is that it opens new pathways to explore the cause of the disease, as well as potential targets for treatment," said Richard Mayeux, co-director of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, and one of the authors of the paper.