The new Alzheimer's disease studies have immediate implications for developing treatments.
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 longstanding question and has immediate implications for developing treatments, researchers said. They said they also suspect that other degenerative brain diseases, such as 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 areas of the brain that involve remembering and reasoning.
But for more than 25 years, researchers have been unable to decide between two explanations. The spread may mean 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 some brain areas are more resilient than others and so resist the disease longer.
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The new studies provide an answer and indicate it may be possible to bring a patient’s Alzheimer’s disease to an abrupt halt early by preventing this cell-to-cell transmission, perhaps with an antibody that blocks tau.
The studies, done independently by 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, not people, researchers say they expect the same phenomenon occurs in humans.
One study, by Karen Duff and Dr. Scott Small and colleagues at the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University, was published Wednesday in the journal PLoS One. The other, by Dr. Bradley Hyman, director of the Alzheimer’s Disease Research Center at Massachusetts General Hospital, and colleagues, is in the journal Neuron.
Both groups 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 differs from tau. It is secreted and clumps outside cells. Researchers 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, piling up inside cells and killing them.