Alzheimer's disease seems to spread like an infection from brain cell to brain cell, two new studies find. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau.

The surprising finding answers a long-standing question and has immediate implications for developing treatments, researchers said. And, they said, they suspect that other degenerative brain diseases, like Parkinson's, may spread in the brain in a similar way.

Alzheimer's researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas of the brain that involve remembering and reasoning.

But for more than a quarter-century they have been unable to decide between two explanations. The spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and so resist the disease longer.

The new studies provide an answer. And they indicate that it may be possible to bring a patient's Alzheimer's disease to an abrupt halt very early in its course by preventing this cell-to-cell transmission, perhaps with an antibody that blocks tau.

The studies, done independently by researchers at Columbia and Harvard Universities, involved genetically engineered mice that could make abnormal human tau proteins, but predominantly in the entorhinal cortex, a sliver of tissue behind the ears, toward the middle of the brain, where cells first start dying in Alzheimer's disease.

As expected, tau showed up there. And, as expected, entorhinal cortex cells in the animals started dying, filled with tangled, spaghettilike strands of tau.

Over the next two years, the cell death and destruction spread outward to other cells that are part of the same nerve cell network. Since those other cells could not make human tau, the only way they could get the protein was by transmission from nerve cell to nerve cell.

And that, said Dr. Sam Gandy, associate director of the Alzheimer's Disease Research Center at Mount Sinai School of Medicine in New York City, was "very unexpected, very intriguing."

Although the studies were in mice, researchers say they expect that the same phenomenon occurs in humans because the mice had a human tau gene and the progressive wave of cell death matched what they see in people with Alzheimer's disease.

One report, by Karen Duff and Dr. Scott Small and their colleagues at the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University, appeared Wednesday in the journal PLoS One. The other, by Dr. Bradley T. Hyman, director of the Alzheimer's Disease Research Center at Massachusetts General Hospital, and his colleagues, is in the journal Neuron.

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