Without its chaperones, the amyloid protein settles in the brain and eventually clusters into plaques.
Levels of the beta amyloid protein naturally rise and fall over 24 hours in both mice and people.
Pepys decided to go after a protein called serum amyloid P (SAP), which glues the amyloid protein together into clumps.
Both drugs are monoclonal antibodies that are supposed to attach to the amyloid protein and clear it from the brain.
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.
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.
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.
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.
To be specific, Merck (MRK) will test a beta-amyloid precursor protein site-cleaving enzyme, or BACE, inhibitor, which the drugmaker notes is the first drug with this type of mechanism to advance to this stage of clinical research.
Beta amyloid is a protein fragment that collects in clumps inside the brains of Alzheimer's patients.
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.
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.
"In my view, these results are very, very slightly hopeful, but not more than this, " says John Hardy, a University College, London, neuroscientist and geneticist who was among the first to point to a link between amyloid, the protein bapineuzumab attacks, and 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.
Increasingly, scientists believe that a protein called amyloid peptide is the culprit in Alzheimer's disease.
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.
It isn't clear how the treatment helps Alzheimer's patients, but it appears to take advantage of antibodies from the plasma donors that combat a protein called amyloid, which clumps in the brains of people with the ailment.
The drugs aim to remove aberrant protein clumps called amyloid plaques from the brains of Alzheimer's patients.
It has been known for a long time that mutations in a protein can encourage amyloid formation.
It binds not just to tau, but also to another protein called beta amyloid, which is commonly seen in Alzheimer's disease patients.
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.
The drug has attracted intense interest because it is one of the first compounds aiming to block protein clumps called amyloid from accumulating in the brains of Alzheimer's patients.
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.
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.
Most scientists believe that Alzheimer's disease is linked to a protein called beta-amyloid.
It trained the patient's own immune system to attack a protein called beta-amyloid that many scientists believe is implicated in Alzheimer's.
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.
They will be widely viewed as a referendum on the prevailing theory in Alzheimer's drug development, which focuses on sticky clumps of protein known as beta amyloid that build up in the brain.
Stability in the alpha helices, even if it decreased the overall stability of the protein, inhibited the formation of amyloid fibrils.
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.
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