"There basically are two prongs and we need to deal with both," said lead researcher Karen Ashe, a University of Minnesota neurologist. "What we're showing is that there are neurons which are affected (by Alzheimer's) but not dead."
New research shows a mutant protein named tau is poisoning brain cells, and that blocking its production may allow some of those sick neurons to recover. It worked in demented mice who, to the scientists' surprise, fairly rapidly regained memory.
There are no drugs yet to block tau, and most of the recent search for Alzheimer's treatments has focused instead on another protein, called beta-amyloid.
But Thursday's study, published in the journal Science, is sure to refocus attention on finding ways to attack this second culprit, too.
It's important research because it bolsters the notion of targeting those sick neurons in hopes of one day reversing at least some of dementia's damage, said William Thies, scientific director of the Alzheimer's Association. Today's Alzheimer's drugs only treat symptoms.
No one knows exactly what causes Alzheimer's, a creeping brain degeneration that afflicts about 4.5 million Americans and is on the rise as the population ages.
The leading theory is that something spurs abnormal production of beta-amyloid, which forms sticky clumps that coat brain cells and kill them — plaque that is the disease's hallmark. But tau clearly plays some role: A mutant form of this protein forms fibrous tangles in brain cells of Alzheimer's patients, and tau seems to be primarily responsible for another form of dementia.
To see if the tangles themselves are a cause or symptom of dementia, Ashe and colleagues specially engineered a mouse to mimic the kind of tau-and-tangle formation seen in Alzheimer's patients' brains.