Alzheimer's Vaccine Gets Second Wind
New Clues Point to Safer Vaccine, Effective Treatment
Big help comes from another research group led by JoAnne McLaurin, PhD, at Canada's University of Toronto. This team was the first to show that the Elan vaccine could improve Alzheimer's symptoms in mice. Now they have the found the key to why the vaccine works, why it causes brain inflammation, and -- most important -- how it might be improved.
In the same issue of Nature Medicine, the McLaurin team reports that a small piece of Aß42 -- Aß4-10 -- raises the same plaque-stopping antibodies as the larger molecule. And in mouse studies, it doesn't cause brain inflammation. Some part of the larger molecule apparently triggers immune responses linked to inflammation.
McLaurin says it looks like the small segment of amyloid protein attacked by anti-Aß4-10 antibodies may be the main troublemaker in Alzheimer's disease. This target appears to be essential for amyloid to self-assemble into plaque.
"The theory -- and I stress that this is only a theory -- is that the anti-Aß4-10 antibody targets an amyloid assembly product, and by pricking out this one product you stop neuronal loss," McLaurin tells WebMD.
It may be that using Aß4-10 as a vaccine would be safer and as effective as the previous version of the Elan vaccine. On the other hand, Nitsch says, it might be better to treat patients with antibody itself -- a strategy known as passive immunization. Or it might be possible to give the vaccine along with drugs to prevent brain inflammation.
McLaurin's team is working on another approach. They're looking for a small molecule that mimics anti-Aß4-10 antibodies. The hope is that such a drug would be small enough to penetrate the brain and stop Alzheimer's disease cold in its tracks. And since people vary enormously in their response to vaccines, an anti-Aß4-10-like drug likely would work for more patients.
What kind of hope does this offer for people who have Alzheimer's disease today? McLaurin warns that research is still in its early stages, but she holds out hope that this approach might work.
"Someone who has florid Alzheimer's disease right now is probably too far along," she says. "But someone in the early stages of the disease has potential to be in clinical trials that will come along. Potentially it will halt the disease -- but it won't bring back anything that they have lost."-->