Researchers found that mice retained memory function, had an average lifespan, and were less prone to seizures.

Reducing levels of the protein tau can prevent seizures and neurological deficits related to Alzheimer’s disease, according to scientists at the Gladstone Institute of Neurological Disease (GIND). They found that when tau is removed from mice genetically engineered to simulate this disease, their memory function is retained and they live a normal lifespan. Reducing tau levels also made mice more resistant to epileptic seizures, they add.

“We wanted to pursue a complementary strategy and try to make the brain more resistant to amyloid-beta proteins without having to change the levels of amyloid-beta itself,” explains the study’s lead author, Erik Roberson, M.D., Ph.D., GIND staff scientist and assistant professor of neurology at University of California, San Francisco. “Amazingly, even partial reduction of tau prevented memory problems and premature deaths in our Alzheimer’s mice, even though their brains were full of amyloid-beta.”

The Gladstone team used a mouse model of Alzheimer’s in which memory deficits are triggered by a human gene that causes overproduction of amyloid-beta. They report that the key finding was that cognitive and neuronal deficits in these mice were prevented when one or both copies of the tau gene were eliminated.

The team say that the breakthrough came when they identified a mechanism by which tau reduction could protect the brain. They found that reducing this protein shields brain cells against overstimulation, which can interfere with the brain’s normal functioning and even cause seizures.

The results were reported in Science.

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