TUESDAY, July 13 (HealthDay News) -- Several new studies to be presented Tuesday at a major Alzheimer's conference describe progress in a series of immune-based therapies that target the tau protein, one of the two major proteins implicated in Alzheimer's disease.
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As a focus of research, tau protein "tangles" have typically taken a backseat to another protein, the beta amyloid plaques that proliferate in the brains of people with Alzheimer's.
However, the new studies suggest that not only do some tau-focused therapies show promise, some treatments targeted against beta amyloid also affect tau.
William Thies, chief medical and scientific officer at the Alzheimer's Association, called the new results "encouraging."
"These are two landmark lesions associated with Alzheimer's. We had thought that affecting one would affect the other," he said. "This suggests we're getting at the heart of the science, though we still have to show that [these approaches] reduce symptoms."
But another expert added a note of caution.
Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City, said that although attempts to battle beta amyloid and tau might yield treatment results down the line, both deposits "may be manifestations of the disease and not its origin." That comes back to a basic science question plaguing the Alzheimer's field: Do these protein accumulations actually cause Alzheimer's, or are they merely a result of another process?
Also, only one of the studies presented at the meeting was conducted in humans and only 10 humans at that -- meaning that the results should be considered very preliminary.
Still, scientists continue to unravel the mystery of Alzheimer's and what it does to the brain. There are currently no curative treatments for this form of dementia, which affects millions of people worldwide.
The findings, from American and international teams of researchers, are slated for presentation at the Alzheimer's Association's International Conference on Alzheimer's Disease 2010 in Honolulu.
Two studies presented together found that treatments aimed at beta amyloid plaques might also tackle tau.
In one study, an antibody known as bapineuzumab -- which actually aims for beta amyloid plaques -- also reduced levels of an abnormal form of tau known as phospho-tau (P-tau) in spinal fluid. The study authors reported ties with drug makers Elan Pharmaceuticals, Janssen Alzheimer Immunotherapy and Pfizer.
Similarly, a second presentation showed that a compound known as AN1792 (made by Elan), by attacking beta amyloid plaques, also was associated with reductions in tau levels.
This trial involved continued follow-up on 10 patients involved in a trial that was halted in 2002 after some participants developed symptoms of brain inflammation.
All 10 patients had been immunized with AN1792. They were compared with 28 Alzheimer's patients who had not been immunized.
And finally, two other animal studies looked at immunization targeted directly at the tau protein.
One found that "passive immunization" with a compound known as the PHF1 antibody not only decreased tau levels but also symptoms in mice.
The study was partially supported by Applied Neurosolutions Inc. and the Alzheimer's Association.
And a group of European researchers reported developing a new rat model that enables researchers to study tau neurofibrillary tangles.
When immunized with an early version of a tau vaccine, the rats showed decreases in tau tangles with associated improvements in functioning, the researchers said.
But again, Kennedy cautioned that the promise from this type of research may still not pan out.
While he believes that this type of study should be pursued, "a lot of us think that both beta amyloid and tau are a blind alley, that something farther upstream may be causing Alzheimer's," Kennedy said.
There is another problem with the approach, though, in that humans make amyloid and tau normally. "Immunizing against naturally occurring natural constituents of the brain, it is a risk," Kennedy said.
Copyright © 2010 HealthDay. All rights reserved.
SOURCES: William Thies, Ph.D., chief medical and scientific officer, Alzheimer's Association; Gary Kennedy, M.D., director of geriatric psychiatry, Montefiore Medical Center, New York, N.Y.; July 13, 2010, presentations, International Conference on Alzheimer's Disease 2010, Honolulu
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