But the fact that it, too, is a brain protein is interesting.
In the late 1980s circumstantial evidence condemning the role of Alzheimer's amyloid plaques began to build when Harvard biologist Bruce Yankner showed, in test tubes, that the amyloid protein poisoned brain cells.
In the late 1980s circumstantial evidence that condemned the role of Alzheimer's amyloid plaques began to build when Bruce Yankner, a Harvard biologist, showed in test tubes that the amyloid protein poisoned brain cells.
There may be an optimal level of protein production inside brain cells needed for learning.
Another is that something else causes the lesions, and the tau protein is the brain's defence against that attack.
On emerging from hibernation, the squirrel eliminates the tau protein from its brain.
"It's not clear exactly how protein clumps damage brain cells, " says Pepys.
Professor Holtzman said the result implied that apoE and clusterin worked together to suppress plaque formation by clearing amyloid protein from the brain tissue and surrounding fluid.
The main anatomical symptoms of Alzheimer's are the growth in the brain of plaques of a protein called beta amyloid, and tangles inside cells of a second protein called tau.
The dominant explanation of Alzheimer's disease contends that the massive brain cell death is due to the buildup of plaques containing a protein called beta amyloid built up in the brain.
Without its chaperones, the amyloid protein settles in the brain and eventually clusters into plaques.
An autopsy found her brain shriveled and filled with strange protein deposits.
But as yet there is no smoking gun - a protein involved in regulating brain function, say - that may have caused our ape-like ancestors to branch off from chimps.
The retinal nerve fiber layer is the one part of the brain where nerve cells are not covered with the fat and protein sheathing called myelin, making this assessment specific for nerve damage as opposed to brain MRI changes, which reflect an array of different types of tissue processes in the brain.
It revealed that healthy brain stem cells displayed a certain telltale protein called CD133 on their surface.
In 2001 researchers at Columbia University and ucla showed in mouse experiments that MTOR drugs compensated for the loss of a protein mutated in prostate and brain cancers.
The mice who lacked apoE and clusterin showed signs of higher levels of amyloid protein not only in their brain tissue, also in the fluid surrounding individual brain cells and the fluid surrounding the entire brain.
He argues that the amount of amyloid in patient brains doesn't correlate much with dementia, and blocking tau, a second protein that accumulates in the brain cells of demented patients, as his company is doing is a much better way to go.
Dr Arendt's group is now engaged in discovering exactly how the tau protein can be cleared from the brain.
One possibility is that the tau protein causes the lesions in the brain.
Both drugs are monoclonal antibodies that are supposed to attach to the amyloid protein and clear it from the brain.
Most researchers are focusing on blocking the formation of amyloid-beta protein or removing it from the brain, either before or after deposits are formed.
Her experiments suggest that blocking the protein hit by gamma secretase will kill brain cells over the long term.
Preventing these gobs of protein debris from wreaking havoc inside the brain may someday help fight not only Alzheimer's disease, but also Huntington's, Lou Gehrig's and Parkinson's.
He argues that the brain is armed with mechanisms for clearing the tau protein and that the reason it doesn't in people with Alzheimer's disease is because the protein is protecting the neurons.
Harvard University researchers conducted experiments on mice using oligomers, a soluble form of amyloid-beta protein, which is the key compound in brain plaque and a hallmark of Alzheimer's.
This has led Dr Arendt to suggest that rather than being a part of a disease process, the formation of the tau protein could be a mechanism by which the brain protects itself.
Moreover, the particular protein that the flies lack is most concentrated in brain areas involved in learning and memory.
Instead, scientists believe that it "recruits" another natural protein, PrP, which sits on the surface of brain cells, to become like it.
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