As expected, the vaccine created antibodies that prevented beta amyloid plaques from forming.
Beta amyloid forms sticky plaques in the brains of Alzheimer's patients and many scientists suspect that slowing plaque formation could slow the disease.
One large area of research is in plaques of beta amyloid which form on the brain.
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.
Amyloid-beta is a precursor of full-blown plaques and, ultimately, dementia.
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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.
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.
"There is a 50-60 percent decrease in the amount of amyloid plaques and indeed the amount of a-beta proteins in the brains of mice who have gotten chronic nasal treatment, " their report said.
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This idea is supported by a study published in April in the Annals of Neurology, which showed that mice without plaques, but with floating beta-amyloid, were just as weakened by the disease as mice with both.
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.
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