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New Strategy Identified for Preventing Acute and Chronic Brain Disease

Scientists at the Gladstone Institute of Neurological Disease (GIND) have discovered that reducing levels of the protein tau can prevent seizures and neurological deficits related to Alzheimer's disease. The findings, reported today in the journal Science, demonstrate that when tau is removed from mice genetically engineered to simulate Alzheimer's disease, their memory function is retained and they live a normal lifespan. Reducing tau levels also made mice more resistant to epileptic seizures.

"This is the most striking therapeutic effect I have ever seen in our disease models," said Lennart Mucke, MD, GIND director and professor of neurology at the University of California, San Francisco (UCSF), and senior author of the study. "A lot more work needs to be done, of course. But if this strategy also works in humans, it could enable a major leap forward in our ability to treat and prevent devastating neurological diseases."

Although Alzheimer's disease (AD) was first described over a hundred years ago, there is still no effective way to prevent it. Many investigational therapies for AD aim to reduce levels of amyloid-beta proteins (AB) because Amyloid-beta builds up to abnormally high levels in the brains of people with AD and is widely suspected to cause the disease.

"We wanted to pursue a complementary strategy and try to make the brain more resistant to A-Beta without having to change the levels of A-Beta itself," said the study's lead author, Erik Roberson MD, PhD, Gladstone staff scientist and assistant professor of neurology at UCSF. "Amazingly, even partial reduction of tau prevented memory problems and premature deaths in our Alzheimer mice, even though their brains were full of amyloid beta."

The Gladstone team used a mouse model of AD in which memory deficits are triggered by a human gene that causes overproduction of A-Beta. The key finding was that cognitive and neuronal deficits in these mice were
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