AD is the most common form of dementia and there is as yet no effective way of preventing it. It is thought that the build-up of amyloid-beta proteins (AB) in people's brains is the cause of AD.
In tests on mice genetically engineered to simulate AD, the research team discovered that when tau was removed their memory function was retained and they lived a normal life span.
When one of both copies of the tau gene were eliminated the cognitive and neuronal deficits in these mice were prevented. Mice with reduced tau levels were also resistant to epileptic seizures.
Lennart Mucke, director of the Gladstone Institute of Neurological Disease at UCSF, said that the findings showed "the most striking therapeutic effect I have ever seen in our disease models".
"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," he added. "There is an urgent need for better treatments in this field, so it is really exciting to have identified such a promising approach."
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