New Treatments for Alzheimer's on the Horizon

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It could be that Dimebon neutralizes then expels the excess amyloid from the brain, or that there is actually some benefit to having amyloid outside the neuron as opposed to inside (where it might be more toxic), Gandy postulated.

And it's entirely possible that beta amyloid is not the main culprit in Alzheimer's. "It's not clear that amyloid is what's toxic to the neurons and it may be that Dimebon is mobilizing the stuff to get it out of the system," said Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City. "Amyloid may be a nasty traveling companion rather than the assassin."

There has been no hint yet that the elevation in beta amyloid levels produces undesirable side effects.

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Pharmaceutical companies are working aggressively to move this drug towards a U.S. Food and Drug Administration approval, said Dr. Ralph Nixon, vice chair of the Alzheimer's Association Medical & Scientific Advisory Council.

"Especially if the drug is confirmed to be efficacious in Phase 3 trials, I think this will be a very strong tool to find clues as to what the basic cause of the disease is and some of the factors leading to the development of Alzheimer's," Nixon said. "Some of those factors may be independent of beta amyloid but it's too early to say that. But it certainly raises some interesting thinking about possible other factors that might be targetable as new drug therapies."

A second study found that a vaccine that targets the neurofibrillary "tau" tangles seen in Alzheimer's brains did actually reduce levels of the structure, at least in mice.

Until now, researchers haven't had much success with amyloid immunization or even with previous experiments with tau vaccines, which have caused brain inflammation in past research.

The Israeli researchers immunized mice who had been genetically engineered to develop neurofibrillary tangles with a combination of three phosphorylated-tau peptides, or shortened versions of the protein.

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