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.
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.
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.
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.
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.
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.
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.
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