However, the protein forms permanent plaques in Alzheimer's disease.
The drugs aim to remove aberrant protein clumps called amyloid plaques from the brains of Alzheimer's patients.
A-beta is a section of protein which, if cut free in its entirety from its parent protein, ends up in plaques.
The technology works by attaching a radioactive marker, called thioflavin, to the tangles of protein, known as amyloid plaques, that are found in the brains of patients with Alzheimer's.
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 the protein, some believe, the plaques that form in the brains of Alzheimer's patients would not exist.
Without the protein, some posit, the plaques that form in the brains of Alzheimer's patients would not exist.
The physical manifestations of the disease that Alois Alzheimer noticed in 1906 are sticky plaques of one type of protein, now known as beta-amyloid, and nerve-cell-engulfing tangles of a second type, called tau protein.
Without its chaperones, the amyloid protein settles in the brain and eventually clusters into plaques.
Most researchers still believe beta-amyloid is the culprit, but the idea that free-floating protein molecules, rather than the proteins in the plaques, are to blame is gaining ground.
Its causes have long been unknown, but increasing circumstantial evidence points to a toxic protein called amyloid peptide, which builds up into plaques and slowly chokes off brain cells.
Other researchers had identified several related protein fragments, called beta-amyloids, inside the amyloid plaques, but they didn't know which proteins were the bad ones.
Other researchers had identified several related protein fragments, called beta-amyloid, inside the amyloid plaques, but they didn't know which proteins were the bad ones.
AN-1792 was a vaccine that immunized patients against a protein called beta amyloid, which is the main component of the plaques that destroy the brain in Alzheimer's disease.
It aims to muffle the gene for a protein called apoliprotein B, or ApoB, that carries fatty cholesterol to the arteries, creating thick plaques.
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.
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