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 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 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 (pronounced en-toh-RYE-nal), 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, spaghetti-like 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, not people, 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 study, 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, was published on 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 Neuron.

Both groups of researchers were inspired by the many observations over the years that Alzheimer's starts in the entorhinal cortex and spreads.

But, said Small, "What do we mean by 'spreads?' " Researchers knew that something sets off Alzheimer's disease; the most likely candidate is a protein known as beta amyloid, which accumulates in the brain of Alzheimer's patients, forming hard, barnaclelike plaques.

But beta amyloid is very different from tau. It is secreted and clumps outside cells. Although researchers have looked, they have never seen evidence that amyloid spreads from cell to cell in a network. But amyloid creates what amounts to a bad neighborhood in memory regions of the brain. Then tau comes in – some researchers call it "the executioner" – piling inside cells and killing them.

If some cells take longer than others to succumb to the bad neighborhood, that would explain the spread of the disease in the brain, and there would be no need to blame something odd, like the spread of tau from cell to cell.

Studies in humans, though, could not determine whether that hypothesis was correct. They involved autopsy studies and brain imaging studies and were "indirect and inconclusive," Small said.

Looking at brains of people who died of the disease, Duff said, is like looking at a wrecked car and trying to figure out what caused the accident. Faulty brakes? Broken struts?

The question of which hypothesis was correct – tau spreading cell to cell, or a bad neighborhood in the brain and different cells with different vulnerabilities to it – remained, dangling and unanswerable. Hyman said he tried for 25 years to find a good way to address it.

One of his ideas was to find a patient or two who happened to have a stroke or other brain injury that severed the entorhinal cortex from the rest of the brain. Then, if such a patient developed Alzheimer's in the entorhinal cortex and it remained contained there, he would have evidence that the disease spread like an infection. But he never could find such patients.

The solution came when science advanced enough for researchers to develop genetically engineered mice that expressed abnormal human tau, but only in their entorhinal cortexes. Those mice, said John Hardy, an Alzheimer's researcher at University College London who was not involved in either study, offered "the cleanest" way to get an answer.

There is another advantage, too, Hyman said. The mice give him a tool to test ways to block tau's spread – and that, he added, "is one of the things we're excited about."

Now, Hardy said, with the mouse studies, the issue of a bad neighborhood is settled. "The answer for tau in Alzheimer's disease is that isn't possible,'" he said.

"That is what is different between these papers and all the others," Hardy said. "It isn't a bad neighborhood. It is contagion from one neuron to another."

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