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The newest thinking is that the two proteins play a tandem role, with amyloid-run-amok the trigger for disease to start brewing years before it becomes apparent. Tau makes its entrance later, as symptoms appear.
Strings of an abnormal form of tau build up inside dying nerve cells. It's called ptau, or phosphorylated tau. When the cells die, the ptau is released into spinal fluid, where it can be measured. Goate knew that spinal tap studies show healthy people have low ptau levels and people with Alzheimer's disease have higher but also variable ptau levels.
In people with particularly high ptau levels in their spinal fluid, her team uncovered a variation in a gene involved in producing the abnormal tau. Then they had to test if that mattered.
Tracking records of several hundred Alzheimer's patients, they found up to a sevenfold difference in how quickly people declined if they had the abnormal genetic marker.
"What you predict from this data is people with lowest levels of tau progress the slowest," said Goate, who reported the work last week in the journal PLoS Genetics.
This genetic work may help the hunt for better Alzheimer's drugs in a different way, by allowing researchers to test experimental therapies in patients who may show an effect the soonest, says William Thies of the Alzheimer's Association. He cautions that spinal taps for now are reserved for research studies.
TauRx is thought to have the drug farthest along in development for breaking up tau tangles, but the company didn't say how soon its next-phase testing could begin. At an international Alzheimer's meeting in Hawaii last summer, other researchers reported that new ways of targeting amyloid might in turn lower tau levels, too -- and that vaccine-like therapies to attack tau are just beginning to be tested in mice.
Lauran Neergaard covers health and medical issues for The Associated Press in Washington.
Copyright 2010 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
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