If beta amyloid is the key to stopping Alzheimer's, dimebon shouldn't work at all.
Beta amyloid is a protein fragment that collects in clumps inside the brains of Alzheimer's patients.
One large area of research is in plaques of beta amyloid which form on the brain.
Elan's other approach would be to inject patients with antibodies for beta amyloid made outside the body.
But we don't know if what is lighting up is tau alone, or beta amyloid, or both.
Levels of the beta amyloid protein naturally rise and fall over 24 hours in both mice and people.
Gandy decided to look at another reputed culprit in Alzheimer's called beta amyloid.
As expected, the vaccine created antibodies that prevented beta amyloid plaques from forming.
Perhaps these compounds will finally prove or disprove the beta amyloid hypothesis.
FORBES: For Pfizer-JNJ Alzheimer's Drug, It May Be Too Late To Try
It binds not just to tau, but also to another protein called beta amyloid, which is commonly seen in Alzheimer's disease patients.
Beta amyloid forms sticky plaques in the brains of Alzheimer's patients and many scientists suspect that slowing plaque formation could slow the disease.
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 antibodies seem to respond to only a quarter of the beta amyloid molecule, and the rest of the molecule seems to call the T cells into action.
Given that bapi seems to be effective in lowering AD biomarkers such as beta amyloid and phospho-tau, perhaps bapi needs to be administered to patients at an earlier stage.
FORBES: For Pfizer-JNJ Alzheimer's Drug, It May Be Too Late To Try
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.
Friedhoff and Buxbaum have shown two things: First, they showed that lovastatin could prevent cells from making beta amyloid in the test tube in doses that could be realistically given to patients.
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.
If bapi is doing what it is supposed to in terms of reducing the levels of beta amyloid and phospho-tau, and yet not improving cognition nor reversing brain shrinkage, perhaps the whole amyloid hypothesis is flawed.
FORBES: For Pfizer-JNJ Alzheimer's Drug, It May Be Too Late To Try
Prions, beta-amyloid and synuclein, by contrast, are full of sticky structures called beta-sheets that react willy-nilly with crucial proteins.
Researchers are still trying to prove the beta-amyloid theory as the cause of AD.
The kinds of tests that would detect beta-amyloid levels are not widely available.
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.
The team also looked at levels of beta-amyloid in the brains.
They used a modified version of the HIV virus to transfer a gene for neprilysin to neurons of genetically modified mice which produced human beta-amyloid.
The treatment also eliminated damage linked to the build-up of beta-amyloid.
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