In a breakthrough, scientists blame tau proteins for spreading Alzheimer's

After more than 25 years of debate, researchers in two separate studies have determined that messed-up tau proteins spread Alzheimer's disease from brain cell to brain cell. And they envision a future treatment that could block tau and stop the disease from worsening.

The New York Times reported details of both studies. PLoS One published the Columbia University Medical Center finding and the journal Neuron will run with the Harvard/Massachusetts General Hospital finding. In a third related study, scientists at the University of Texas Medical Branch at Galveston released research reinforcing how significant tau is to Alzheimer's. That paper is published in FASEB Journal.

Scientists in the Columbia and Harvard studies believe the results are true for people because they used genetically engineered mice that expressed the abnormal human tau cells, according to the Times story. And while beta amyloid protein has long been known to build up in Alzheimer's patients' brains, the studies seem to suggest it is more of a first wave of trouble, before the damaged tau travels to the region and kills the brain cells outright, the NYT notes. A lot more research will be necessary to reinforce the finding, but it is a hopeful discovery that points to a potential way to stop the disease, assuming the damaged tau can be prevented from spreading.

As the University of Texas explains, tau proteins function in normal brains in individual units that help promote healthy, functioning neurons. But Alzheimer's brains contain distorted, dying tau proteins twisted into "neurofibrillary tangles." Researchers have long known the messed up tau cells are a big sign of Alzheimer's, appearing in the part of the brain that experiences and stores memory. But their studies helped them realize how important the bad tau proteins are in spreading the disease.

Once again, genetically engineered mice came to the rescue. Scientists in both the Columbia and Harvard studies engineered them to make the abnormal human tau proteins near the middle portion of the brain, where Alzheimer's first starts killing cells. They tracked the formation of the neurofibrillary tangles, as expected, but also noticed over two years that the Alzheimer's-related cell damage spread to other brain cells along the same network from neuron to neuron, thanks to the damaged tau.

- here's the NYT story
- read the University of Texas release
- check out the abstract in PLoS ONE

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